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"Everyone in the field of nutrition science stands on the shoulders
of Dr. Campbell, who is one of the giants in the field. This is one
of the most important books about nutrition ever written —
reading it may save your life."

— Dean Ornish, MD

The Most Comprehensive Study
of Nutrition Ever Conducted

THE

CHINA

STUDYi

Startling Implications for Diet,
Weight Loss and Long-term Health

T. Colin Campbell, PhD
and Thomas M. Campbell ii

FOREWORD BY JOHN ROBBINS, AUTHOR, DlET FOR A NEW AMERICA

PRAISE FOR THE CHINA STUDY

"The China Study gives critical, life-saving nutritional information for ev-
ery health-seeker in America. But it is much more; Dr. Campbell's expose
of the research and medical establishment makes this book a fascinating
read and one that could change the future for all of us. Every health care
provider and researcher in the world must read it."

— Joel Fuhrman, M.D.
Author of the Best-Selling Book, Eat To Live

"Backed by well-documented, peer-reviewed studies and overwhelming
statistics the case for a vegetarian diet as a foundation for a healthy life-
style has never been stronger."

— Bradly Saul, OrganicAthlete.com

"The China Study is the most important book on nutrition and health to
come out in the last seventy-five years. Everyone should read it, and it
should be the model for all nutrition programs taught at universities.
The reading is engrossing if not astounding. The science is conclusive.
Dr. Campbell's integrity and commitment to truthful nutrition education
shine through."

— David Klein, Publisher/Editor
Living Nutrition Magazine

"The China Study describes a monumental survey of diet and death rates
from cancer in more than 2,400 Chinese counties and the equally monu-
mental efforts to explore its significance and implications for nutrition
and health. Dr. Campbell and his son, Thomas, have written a lively, pro-
vocative and important book that deserves widespread attention."

— Frank Rhodes, Ph.D.
President (1978-1995) Emeritus, Cornell University

"Colin Campbell's The China Study is an important book, and a highly
readable one. With his son, Tom, Colin studies the relationship between
diet and disease, and his conclusions are startling. The China Study is a
story that needs to be heard."

— Robert C. Richardson, Ph.D.
Nobel Prize Winner, Professor of Physics
and Vice Provost of Research, Cornell University

"The China Study is the account of a ground-breaking research study that
provides the answers long sought by physicians, scientists and health-
conscious readers. Based on painstaking investigations over many years,
it unearths surprising answers to the most important nutritional ques-
tions of our time: What really causes cancer? How can we extend our
lives? What will turn around the obesity epidemic? The China Study
quickly and easily dispenses with fad diets, relying on solid and convinc-
ing evidence. Clearly and beautifully written by one of the world's most
respected nutrition authorities, The China Study represents a major turn-
ing point in our understanding of health."

— Neal Barnard, M.D., President
Physician's Committee for Responsible Medicine

"Everyone in the field of nutrition science stands on the shoulders of T.
Colin Campbell, who is one of the giants in the field. This is one of the
most important books about nutrition ever written — reading it may save
your life."

— Dean Ornish, M.D., Founder & President
Preventive Medicine Research Institute Clinical Professor of Medicine,
University of California, San Francisco
Author, Dr. Dean Ornish's Program for Reversing Heart Disease and Love & Survival

"The China Study is the most convincing evidence yet on preventing heart
disease, cancer and other Western diseases by dietary means. It is the
book of choice both for economically developed countries and for coun-
tries undergoing rapid economical transition and lifestyle change."

— Junshi Chen, M.D., Ph.D., Senior Research Professor
Institute of Nutrition and Food Safety,
Chinese Center for Disease Control and Prevention

"All concerned with the obesity epidemic, their own health, and the stag-
gering environmental and social impacts of the Western diet will find
wise and practical solutions in Dr. Campbell's The China Study."

— Robert Goodland, Lead Advisor on the Environment
The World Bank Group (1978-2001)

"Dr. Campbell's book The China Study is a moving and insightful his-
tory of the struggle — still ongoing — to understand and explain the vital
connection between our health and what we eat. Dr. Campbell knows
this subject from the inside: he has pioneered the investigation of the

diet-cancer link since the days of the seminal China Study, the NAS
report, Diet, Nutrition and Cancer and AICR's expert panel report, Food,
Nutrition and the Prevention oj Cancer: A Global Perspective. Consequent-
ly, he is able to illuminate every aspect of this question. Today, AICR
advocates a predominantly plant-based diet for lower cancer risk because
of the great work Dr. Campbell and just a few other visionaries began
twenty-five years ago."

— Marilyn Gentry, President
American Institute for Cancer Research

"The China Study is a well-documented analysis of the fallacies of the
modern diet, lifestyle and medicine and the quick fix approach that often
fails. The lessons from China provide compelling rationale for a plant-
based diet to promote health and reduce the risk of the diseases of afflu-
ence."

— Sushma Palmer, Ph.D., Former Executive Director
Food and Nutrition Board, U.S. National Academy of Sciences

"The China Study is extraordinarily helpful, superbly written and pro-
foundly important. Dr. Campbell's work is revolutionary in its implica-
tions and spectacular in its clarity. 1 learned an immense amount from
this brave and wise book. If you want to eat bacon and eggs for breakfast
and then take cholesterol- lowering medication, that's your right. But if
you want to truly take charge of your health, read The China Study and do
it soon! If you heed the counsel of this outstanding guide, your body will
thank you every day for the rest of your life."

— John Robbins, Author of the Best-Selling Books
Diet for a New America and The Food Revolution

"The China Study is a rare treat. Finally, a world-renowned nutritional
scholar has explained the truth about diet and health in a way that ev-
eryone can easily understand — a startling truth that everyone needs to
know. In this superb volume, Dr. Campbell has distilled, with his son
Tom, for us the wisdom of his brilliant career. If you feel any confusion
about how to find the healthiest path for yourself and your family, you
will find precious answers in The China Study. Don't miss it!"

— Douglas J. Lisle, Ph.D., & Alan Goldhamer, D.C.
Authors of The Pleasure Trap: Mastering the Hidden Force
That Undermines Health and Happiness

"So many diet and health books contain conflicting advice, but most
have one thing in common — an agenda to sell something. Dr. Campbell's
only agenda is truth. As a distinguished professor at Cornell University
Dr. Campbell is the Einstein of nutrition. The China Study is based on
hardcore scientific research, not the rank speculation of a Zone, Atkins,
SugarBusters or any other current fad. Dr. Campbell lays out his lifetime
of research in an accessible, entertaining way. Read this book and you
will know why."

— Jeff Nelson, President
VegSource.com (most visited food Web site in the world)

"If you're looking to enhance your health, performance and your success
read The China Study immediately. Finally, scientifically valid guidance on
how much protein we need and where we should get it. The impact of
these findings is enormous."

— John Allen Mollenhauer, Founder
MyTrainer.com and NutrientRich.com

The China Study

THE

China Study

The Most Comprehensive Study
of Nutrition Ever Conducted
and the Startling Implications
for Diet, Weight Loss
and Long-term Health

T. Colin Campbell, Ph.D.
and Thomas M. Campbell II

BENBELLA BOOKS
Dallas, Texas

Nothing written in this book should be viewed as a substitute for competent medical
care. Also, you should not undertake any changes in diet or exercise patterns without
first consulting your physician, especially if you are currently being treated for any risk
factor related to heart disease, high blood pressure or adult-onset diabetes.

All rights reserved. No part of this book may be used or reproduced in any manner
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The Library of Congress has cataloged the hardcover edition as follow:

Campbell, T. Colin, 1934-

The China study : the most comprehensive study of nutrition ever
conducted and the startling implications for diet, weight loss, and
long-term health / by T. Colin Campbell and Thomas M. Campbell II.

p. cm.
ISBN 1-932100-38-5

L. Nutrition. 2. Nutritionally induced diseases. 3. Diet in disease.
I. Campbell, Thomas M. 11. Title.
RA784.C235 2004
613.2— dc22

Cover design by Melody Cadungog
Text design and composition by John Reinhardt Book Design
Printed by Victor Graphics, Inc.

Distributed by Independent Publishers Group
To order call (800) 888-4741
www.ipgbook.com

First BenBella Books Paperback Edition 2006

mtmtA

ISBN 1-932100-66-0

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Foe special sales contact Robyn White at robyn@benbellabooks.corn

To Karen Campbell, whose incredible love and
caring made this book possible.

And to Thomas Mcllwain Campbell and
Betty DeMott Campbell for their incredible gifts.

Acknowledgements

This book, from its original conception to its final form, was in the making for
many years. But it was the last three that gave the book form. And this hap-
pened because Karen, my lifelong love and wife of forty-three years, made it
so. I wanted to do it, but she wanted it even more. She said it had to be done
for the children of the world. She cajoled, she pushed and she insisted that we
keep our nose to the grindstone. She read every word, those kept and those
discarded — some several times.

Most importantly, Karen first suggested that I work with Tom, the youngest
of our five children. His writing skills, his persistence in keeping integrity with
the message and his exceptionally quick learning of the subject matter made
the project possible. He wrote several chapters in this book himself and rewrote
many more, bringing clarity to my message.

And our other children (Nelson — and wife Kim, LeAnne, Keith, Dan)
and grandchildren (Whitney, Colin, Steven, Nelson, Laura) could not have
been more encouraging. Their love and support cannot be measured in mere
words.

I also am indebted to another family of mine: my many undergraduate hon-
ors students, post-graduate doctoral students, post-doctoral research associates
and my fellow professorial colleagues who worked in my research group and
who were the gems of my career. Regretfully, I could only cite in this book a
small sample of their findings, but far, far more could have been included.

Yet more friends, associates and family contributed mightily, through their
meticulous reading of various versions of the manuscript and their detailed feed-
back. Alphabetically, they included Nelson Campbell, Ron Campbell, Kent Car-
roll, Antonia Demas, Mark Epstein, John and Martha Ferger, Kimberly Kathan,
Doug Lisle, John Robbins, Paul Sontrop and Glenn Yeffeth. Advice, support and
generous help also came in many other forms from Neal Barnard, Jodi Blanco,
Junshi Chen, Robert Goodland, Michael Jacobson, Ted Lange, Howard Lyman,

xii

THE CHINA STUDY

Bob Mecoy, John Allen Mollenhauer, Jeff Nelson, Sushma Palmer, Jeff Prince,
Frank Rhodes, Bob Richardson and Kathy Ward.

Of course, I am grateful to all those at BenBella Books, including Glenn Yef-
feth, Shanna Caughey Meghan Kuckelman, Laura Watkins and Leah Wilson
for turning a messy Word document into the book you now have. In addition,
Kent Carroll added professionalism, understanding and a clear vision with his
valuable editing work.

The heart of this book is the China Study itself. It was not the whole story,
of course, but it was the "tipping point" in the development of my ideas. The
actual study in China could not have happened without the extraordinary lead-
ership and dedicated hard work of Junshi Chen and Li Junyao in Beijing, Sir
Richard Peto and Jillian Boreham at the University of Oxford in England, and
Linda Youngman, Martin Root and Banoo Parpia in my own group at Cornell.
Dr. Chen directed more than 200 professional workers as they carried out the
nationwide study in China. His professional and personal characteristics have
been an inspiration to me; it is his kind of work and persona that makes this
world a better place.

Similarly, Drs. Caldwell Esselstyn, Jr., and John McDougall (and Ann and
Mary, respectively) generously agreed to participate in this book. Their dedica-
tion and courage are inspiring.

All of this was possible, of course, because of the exceptional start given to
me by my parents, Tom and Betty Campbell, to whom this book is dedicated.
Their love and dedication created for me and my siblings more opportunities
than they ever dreamed of having.

I must also credit my colleagues who have worked to discredit my ideas and,
not infrequently, me personally. They inspire in a different way. They compel
me to ask why there is so much unnecessary hostility to ideas that should be
part of the scientific debate. In searching for answers, I have gained a wiser,
more unique perspective that I could not have considered otherwise.

Lastly, I must thank you, the taxpaying American public. You funded my
work for more than four decades, and I hope that in telling you the lessons I've
learned, I can begin to repay my debt to you.

— T. Colin Campbell

In addition to all those listed previously, I acknowledge my parents. My in-
volvement in this book was, and still is, a gift from them I shall cherish for the
rest of my life. Words cannot describe my good fortune in having parents who
are such wonderful teachers, supporters and motivators.

Also, Kimberly Kathan provided support, advice, companionship and pas-
sion for this project. She made the lows bearable and the highs exceptional in
this great roller coaster of an adventure.

— Thomas M. Campbell, II

Contents

Introduction 1

Part I: The China Study

1. Problems We Face, Solutions We Need 11

2. A House of Proteins 27

3. Turning Off Cancer 43

4. Lessons from China 69

Part II: Diseases of Affluence

5. Broken Hearts 111

6. Obesity 135

7. Diabetes 145

8. Common Cancers: Breast, Prostate, Large Bowel

(Colon and Rectal) 157

9. Autoimmune Diseases 183

10. Wide-Ranging Effects: Bone, Kidney, Eye and Brain Diseases 203

Part III: The Good Nutrition Guide

11. Eating Right: Eight Principles of Food and Health 225

12. How to Eat 241

xiii

xiv

CONTENTS

Part IV: Why Haven't You Heard This Before?

13. Science — The Dark Side 251

14. Scientific Reductionism 269

15. The "Science" of Industry 289

16. Government: Is It for the People? 305

17. Big Medicine: Whose Health Are They Protecting? 321

18. Repeating Histories 343

Appendix A. Q&A: Protein Effect in Experimental Rat Studies 351

Appendix B. Experimental Design of the China Study 353

Appendix C. The "Vitamin" D Connection 361

References 369

Preface

T. Colin Campbell, at his core, is still a farm boy from northern Virginia.
When we spend time together we inevitably share our stories from the
farm. Whether it is spreading cow manure, driving tractors or herding
cattle, both of us share a rich history in farming.

But from these backgrounds, both he and I went on to other careers.
It is for his other career accomplishments that I came to admire Colin.
He was involved in the discovery of a chemical later called dioxin, and
he went on to direct one of the most important diet and health studies
ever conducted, the China Study. In between, he authored hundreds
of scientific papers, sat on numerous government expert panels and
helped shape national and international diet and health organizations,
like the American Institute for Cancer Research/World Cancer Research
Fund. As a scientist, he has played an instrumental role in how our
country views diet and health.

And yet, as I have gotten to know Colin on a personal level, I have
come to respect him for reasons other than just his list of professional ac-
complishments. I have come to respect him for his courage and integrity.

Colin seriously questions the status quo, and even though the scien-
tific evidence is on his side, going against the grain is never easy I know
this well because I have been a co-defendant with Oprah Winfrey when
a group of cattlemen decided to sue her after she stated her intention
not to eat beef. I have been in Washington, D.C., lobbying for better
agricultural practices and fighting to change the way we raise and grow
food in this country. I have taken on some of the most influential, well-
funded groups in the country and I know that it's not easy.

xvi

THE CHINA STUDY

Because of our parallel paths, I feel connected to Colin's story. We
started on the farm, learning independence, honesty and integrity in
small communities, and went on to become established in mainstream
careers. Although we both had success (I still remember the first seven-
figure check I wrote for my massive cattle operation in Montana), we
came to realize that the system we lived in could use some improve-
ments. Challenging the system that provided us with such rewards has
demanded an iron will and steadfast integrity Colin has both, and this
book is a brilliant capstone to a long and dignified career. We would do
well to learn from Colin, who has reached the top of his profession and
then had the courage to reach even higher by demanding change.

Whether you have interest in your personal health or in the wretched
state of health in the United States, this book will richly reward you.
Read it carefully, absorb its information and apply it to your life.

— Howard Lyman, author of Mad Cowboy

Foreword

If you are like most Americans today, you are surrounded by fast food
chain restaurants. You are barraged by ads for junk foods. You see other
ads, for weight-loss programs, that say you can eat whatever you want,
not exercise and still lose weight. It's easier to find a Snickers bar, a Big
Mac or a Coke than it is to find an apple. And your kids eat at a school
cafeteria whose idea of a vegetable is the ketchup on the burgers.

You go to your doctor for health tips. In the waiting room, you find
a glossy 243-page magazine titled Family Doctor: Your Essential Guide to
Health and Well-being. Published by the American Academy of Family
Physicians and sent free to the offices of all 50,000 family doctors in the
United States in 2004, it's full of glossy full-page color ads for McDon-
ald's, Dr Pepper, chocolate pudding and Oreo cookies.

You pick up an issue of National Geographic Kids, a magazine pub-
lished by the National Geographic Society "for ages six and up," expect-
ing to find wholesome reading for youngsters. The pages, however, are
filled with ads for Twinkies, M&Ms, Frosted Flakes, Froot Loops, Host-
ess Cup Cakes and Xtremejell-O Pudding Sticks.

This is what scientists and food activists at Yale University call a toxic
food environment. It is the environment in which most of us live today

The inescapable fact is that certain people are making an awful lot of
money today selling foods that are unhealthy. They want you to keep
eating the foods they sell, even though doing so makes you fat, depletes
your vitality and shortens and degrades your life. They want you docile,
compliant and ignorant. They do not want you informed, active and
passionately alive, and they are quite willing to spend billions of dollars
annually to accomplish their goals.

xvii

xviii

THE CHINA STUDY

You can acquiesce to all this, you can succumb to the junk food sellers,
or you can find a healthier and more life-affirming relationship with your
body and the food you eat. If you want to live with radiant health, lean and
clear and alive in your body you'll need an ally in todays environment.

Fortunately you have in your hand just such an ally. T. Colin
Campbell, Ph.D., is widely recognized as a brilliant scholar, a dedi-
cated researcher and a great humanitarian. Having had the pleasure and
privilege to be his friend, I can attest to all of that, and I can also add
something else. He is also a man of humility and human depth, a man
whose love for others guides his every step.

Dr. Campbell's new book — The China Study — is a great ray of light in
the darkness of our times, illuminating the landscape and the realities of
diet and health so clearly so fully that you need never again fall prey to
those who profit from keeping you misinformed, confused and obedi-
ently eating the foods they sell.

One of the many things I appreciate about this book is that Dr. Campbell
doesn't just give you his conclusions. He doesn't preach from on high, tell-
ing what you should and shouldn't eat, as if you were a child. Instead, like
a good and trusted friend who happens to have learned, discovered and
done more in his life than most of us could ever imagine, he gendy clearly
and skillfully gives you the information and data you need to fully under-
stand what's involved in diet and health today. He empowers you to make
informed choices. Sure, he makes recommendations and suggestions, and
terrific ones at that. But he always shows you how he has arrived at his con-
clusions. The data and the truth are what are important. His only agenda is
to help you live as informed and healthy a life as possible.

I've read The China Study twice already, and each time I've learned
an immense amount. This is a brave and wise book. The China Study is
extraordinarily helpful, superbly written and profoundly important. Dr.
Campbell's work is revolutionary in its implications and spectacular in
its clarity.

If you want to eat bacon and eggs for breakfast and then take cho-
lesterol-lowering medication, that's your right. But if you want to truly
take charge of your health, read The China Study, and do it soon! If you
heed the counsel of this outstanding guide, your body will thank you
every day for the rest of your life.

— John Robbins, author of Diet for a New America, Reclaiming Our
Health and The Food Revolution

Introduction

The public's hunger for nutrition information never ceases to amaze me,
even after devoting my entire working life to conducting experimental
research into nutrition and health. Diet books are perennial best-sellers.
Almost every popular magazine features nutrition advice, newspapers
regularly run articles and TV and radio programs constantly discuss
diet and health.

Given the barrage of information, are you confident that you know
what you should be doing to improve your health?

Should you buy food that is labeled organic to avoid pesticide ex-
posure? Are environmental chemicals a primary cause of cancer? Or
is your health "predetermined" by the genes you inherited when you
were born? Do carbohydrates really make you fat? Should you be more
concerned about the total amount of fat you eat, or just saturated fats
and trans-fats? What vitamins, if any, should you be taking? Do you buy
foods that are fortified with extra fiber? Should you eat fish, and, if so,
how often? Will eating soy foods prevent heart disease?

My guess is that you're not really sure of the answers to these ques-
tions. If this is the case, then you aren't alone. Even though information
and opinions are plentiful, very few people truly know what they should
be doing to improve their health.

This isn't because the research hasn't been done. It has. We know an
enormous amount about the links between nutrition and health. But
the real science has been buried beneath a clutter of irrelevant or even
harmful information — junk science, fad diets and food industry propa-
ganda.

THE CHINA STUDY

I want to change that. I want to give you a new framework for under-
standing nutrition and health, a framework that eliminates confusion,
prevents and treats disease and allows you to live a more fulfilling life.

I have been "in the system" for almost fifty years, at the very highest
levels, designing and directing large research projects, deciding which
research gets funded and translating massive amounts of scientific re-
search into national expert panel reports.

After a long career in research and policy making, I now understand
why Americans are so confused. As a taxpayer who foots the bill for re-
search and health policy in America, you deserve to know that many of
the common notions you have been told about food, health and disease
are wrong:

• Synthetic chemicals in the environment and in your food, as prob-
lematic as they may be, are not the main cause of cancer.

• The genes that you inherit from your parents are not the most im-
portant factors in determining whether you fall prey to any of the
ten leading causes of death.

• The hope that genetic research will eventually lead to drug cures
for diseases ignores more powerful solutions that can be employed
today.

• Obsessively controlling your intake of any one nutrient, such as
carbohydrates, fat, cholesterol or omega-3 fats, will not result in
long-term health.

• Vitamins and nutrient supplements do not give you long-term pro-
tection against disease.

• Drugs and surgery don't cure the diseases that kill most Ameri-
cans.

• Your doctor probably does not know what you need to do to be the
healthiest you can be.

I propose to do nothing less than redefine what we think of as good
nutrition. The provocative results of my four decades of biomedical
research, including the findings from a twenty-seven-year laboratory
program (funded by the most reputable funding agencies) prove that
eating right can save your life.

I will not ask you to believe conclusions based on my personal obser-
vations, as some popular authors do. There are over 750 references in this
book, and the vast majority of them are primary sources of information,
including hundreds of scientific publications from other researchers

INTRODUCTION

that point the way to less cancer, less heart disease, fewer strokes, less
obesity, less diabetes, less autoimmune disease, less osteoporosis, less
Alzheimer's, less kidney stones and less blindness.

Some of the findings, published in the most reputable scientific jour-
nals, show that:

• Dietary change can enable diabetic patients to go off their medica-
tion.

• Heart disease can be reversed with diet alone.

• Breast cancer is related to levels of female hormones in the blood,
which are determined by the food we eat.

• Consuming dairy foods can increase the risk of prostate cancer.

• Antioxidants, found in fruits and vegetables, are linked to better
mental performance in old age.

• Kidney stones can be prevented by a healthy diet.

• Type 1 diabetes, one of the most devastating diseases that can be-
fall a child, is convincingly linked to infant feeding practices.

These findings demonstrate that a good diet is the most powerful
weapon we have against disease and sickness. An understanding of this
scientific evidence is not only important for improving health; it also
has profound implications for our entire society. We must know why
misinformation dominates our society and why we are grossly mistaken
in how we investigate diet and disease, how we promote health and how
we treat illness.

By any number of measures, America's health is failing. We spend far
more, per capita, on health care than any other society in the world, and
yet two thirds of Americans are overweight, and over 15 million Ameri-
cans have diabetes, a number that has been rising rapidly We fall prey to
heart disease as often as we did thirty years ago, and the War on Cancer,
launched in the 1970s, has been a miserable failure. Half of Americans
have a health problem that requires taking a prescription drug every
week, and over 100 million Americans have high cholesterol.

To make matters worse, we are leading our youth down a path of dis-
ease earlier and earlier in their lives. One third of the young people in
this country are overweight or at risk of becoming overweight. Increas-
ingly they are falling prey to a form of diabetes that used to be seen only
in adults, and these young people now take more prescription drugs
than ever before.

These issues all come down to three things: breakfast, lunch and dinner.

THE CHINA STUDY

More than forty years ago, at the beginning of my career, I would have
never guessed that food is so closely related to health problems. For years
I never gave much thought to which foods were best to eat. I just ate what
everyone else did: what I was told was good food. We all eat what is tasty or
what is convenient or what our parents taught us to prefer. Most of us live
within cultural boundaries that define our food preferences and habits.

So it was with me. I was raised on a dairy farm where milk was
central to our existence. We were told in school that cow's milk made
strong, healthy bones and teeth. It was Nature's most perfect food. On
our farm, we produced most of our own food in the garden or in the
livestock pastures.

I was the first in my family to go to college. I studied pre-veterinary
medicine at Penn State and then attended veterinary school at the Uni-
versity of Georgia for a year when Cornell University beckoned with
scholarship money for me to do graduate research in "animal nutrition."
I transferred, in part, because they were going to pay me to go to school
instead of me paying them. There I did a master's degree. I was the last
graduate student of Professor Clive McCay, a Cornell professor famed
for extending the lives of rats by feeding them much less food than they
would otherwise eat. My Ph.D. research at Cornell was devoted to find-
ing better ways to make cows and sheep grow faster. I was attempting
to improve on our ability to produce animal protein, the cornerstone of
what I was told was "good nutrition."

I was on a trail to promote better health by advocating the consump-
tion of more meat, milk and eggs. It was an obvious sequel to my own
life on the farm and I was happy to believe that the American diet was
the best in the world. Through these formative years, I encountered a
recurring theme: we were supposedly eating the right foods, especially
plenty of high-quality animal protein.

Much of my early career was spent working with two of the most
toxic chemicals ever discovered, dioxin and anatoxin. I initially worked
at MIT, where I was assigned a chicken feed puzzle. Millions of chicks
a year were dying from an unknown toxic chemical in their feed, and
I had the responsibility of isolating and determining the structure of
this chemical. After two and one-half years, I helped discover dioxin,
arguably the most toxic chemical ever found. This chemical has since
received widespread attention, especially because it was part of the her-
bicide 2,4,5-T, or Agent Orange, then being used to defoliate forests in
the Vietnam War.

INTRODUCTION

After leaving MIT and taking a faculty position at Virginia Tech, I
began coordinating technical assistance for a nationwide project in the
Philippines working with malnourished children. Part of the project
became an investigation of the unusually high prevalence of liver can-
cer, usually an adult disease, in Filipino children. It was thought that
high consumption of aflatoxin, a mold toxin found in peanuts and corn,
caused this problem. Aflatoxin has been called one of the most potent
carcinogens ever discovered.

For ten years our primary goal in the Philippines was to improve
childhood malnutrition among the poor, a project funded by the U.S.
Agency for International Development. Eventually, we established about
110 nutrition "self-help" education centers around the country.

The aim of these efforts in the Philippines was simple: make sure that
children were getting as much protein as possible. It was widely thought
that much of the childhood malnutrition in the world was caused by a
lack of protein, especially from animal-based foods. Universities and
governments around the world were working to alleviate a perceived
"protein gap" in the developing world.

In this project, however, I uncovered a dark secret. Children who ate
the highest-protein diets were the ones most likely to get liver cancer! They
were the children of the wealthiest families.

I then noticed a research report from India that had some very pro-
vocative, relevant findings. Indian researchers had studied two groups
of rats. In one group, they administered the cancer-causing aflatoxin,
then fed a diet that was composed of 20% protein, a level near what
many of us consume in the West. In the other group, they administered
the same amount of aflatoxin, but then fed a diet that was only com-
posed of 5% protein. Incredibly, every single animal that consumed the
20% protein diet had evidence of liver cancer, and every single animal
that consumed a 5% protein diet avoided liver cancer. It was a 100 to 0
score, leaving no doubt that nutrition trumped chemical carcinogens,
even very potent carcinogens, in controlling cancer.

This information countered everything I had been taught. It was
heretical to say that protein wasn't healthy, let alone say it promoted
cancer. It was a defining moment in my career. Investigating such a
provocative question so early in my career was not a very wise choice.
Questioning protein and animal-based foods in general ran the risk of
my being labeled a heretic, even if it passed the test of "good science."

But I never was much for following directions just for the sake of

THE CHINA STUDY

following directions. When I first learned to drive a team of horses or
herd cattle, to hunt animals, to fish our creek or to work in the fields,
I came to accept that independent thinking was part of the deal. It had
to be. Encountering problems in the field meant that I had to figure out
what to do next. It was a great classroom, as any farm boy can tell you.
That sense of independence has stayed with me until today.

So, faced with a difficult decision, I decided to start an in-depth labora-
tory program that would investigate the role of nutrition, especially pro-
tein, in the development of cancer. My colleagues and I were cautious in
framing our hypotheses, rigorous in our methodology and conservative
in interpreting our findings. I chose to do this research at a very basic sci-
ence level, studying the biochemical details of cancer formation. It was
important to understand not only whether but also how protein might
promote cancer. It was the best of all worlds. By carefully following the
rules of good science, I was able to study a provocative topic without pro-
voking knee-jerk responses that arise with radical ideas. Eventually, this
research became handsomely funded for twenty-seven years by the best-
reviewed and most competitive funding sources (mostly the National In-
stitutes of Health (NIH), the American Cancer Society and the American
Institute for Cancer Research). Then our results were reviewed (a second
time) for publication in many of the best scientific journals.

What we found was shocking. Low-protein diets inhibited the initia-
tion of cancer by anatoxin, regardless of how much of this carcinogen
was administered to these animals. After cancer initiation was com-
pleted, low-protein diets also dramatically blocked subsequent cancer
growth. In other words, the cancer-producing effects of this highly car-
cinogenic chemical were rendered insignificant by a low-protein diet. In
fact, dietary protein proved to be so powerful in its effect that we could turn
on and turn off cancer growth simply by changing the level consumed.

Furthermore, the amounts of protein being fed were those that we
humans routinely consume. We didn't use extraordinary levels, as is so
often the case in carcinogen studies.

But that's not all. We found that not all proteins had this effect. What
protein consistently and strongly promoted cancer? Casein, which
makes up 87% of cow's milk protein, promoted all stages of the cancer
process. What type of protein did not promote cancer, even at high lev-
els of intake? The safe proteins were from plants, including wheat and
soy. As this picture came into view, it began to challenge and then to
shatter some of my most cherished assumptions.

INTRODUCTION

These experimental animal studies didn't end there. 1 went on to
direct the most comprehensive study of diet, lifestyle and disease ever
done with humans in the history of biomedical research. It was a mas-
sive undertaking jointly arranged through Cornell University, Oxford
University and the Chinese Academy of Preventive Medicine. The New
York Times called it the "Grand Prix of Epidemiology." This project
surveyed a vast range of diseases and diet and lifestyle factors in rural
China and, more recently, in Taiwan. More commonly known as the
China Study, this project eventually produced more than 8,000 statisti-
cally significant associations between various dietary factors and disease!

What made this project especially remarkable is that, among the
many associations that are relevant to diet and disease, so many pointed
to the same finding: people who ate the most animal-based foods got
the most chronic disease. Even relatively small intakes of animal-based
food were associated with adverse effects. People who ate the most
plant-based foods were the healthiest and tended to avoid chronic dis-
ease. These results could not be ignored. From the initial experimental
animal studies on animal protein effects to this massive human study
on dietary patterns, the findings proved to be consistent. The health
implications of consuming either animal or plant-based nutrients were
remarkably different.

I could not, and did not, rest on the findings of our animal studies
and the massive human study in China, however impressive they may
have been. 1 sought out the findings of other researchers and clinicians.
The findings of these individuals have proved to be some of the most
exciting findings of the past fifty years.

These findings — the contents of Part II of this book — show that heart
disease, diabetes and obesity can be reversed by a healthy diet. Other
research shows that various cancers, autoimmune diseases, bone health,
kidney health, vision and brain disorders in old age (like cognitive dys-
function and Alzheimer's) are convincingly influenced by diet. Most im-
portantly, the diet that has time and again been shown to reverse and/or
prevent these diseases is the same whole foods, plant-based diet that I
had found to promote optimal health in my laboratory research and in
the China Study. The findings are consistent.

Yet, despite the power of this information, despite the hope it gener-
ates and despite the urgent need for this understanding of nutrition and
health, people are still confused. I have friends with heart disease who
are resigned and despondent about being at the mercy of what they

THE CHINA STUDY

consider to be an inevitable disease. I've talked with women who are so
terrified of breast cancer that they wish to have their own breasts, even
their daughters' breasts, surgically removed, as if that's the only way to
minimize risk. So many of the people I have met have been led down a
path of illness, despondence and confusion about their health and what
they can do to protect it.

Americans are confused, and I will tell you why. The answer, dis-
cussed in Part IV, has to do with how health information is generated
and communicated and who controls such activities. Because I have
been behind the scenes generating health information for so long, I
have seen what really goes on — and I'm ready to tell the world what is
wrong with the system. The distinctions between government, indus-
try, science and medicine have become blurred. The distinctions be-
tween making a profit and promoting health have become blurred. The
problems with the system do not come in the form of Hollywood-style
corruption. The problems are much more subtle, and yet much more
dangerous. The result is massive amounts of misinformation, for which
average American consumers pay twice. They provide the tax money to
do the research, and then they provide the money for their health care
to treat their largely preventable diseases.

This story, starting from my personal background and culminating
in a new understanding of nutrition and health, is the subject of this
book. Six years ago at Cornell University, I organized and taught a new
elective course called Vegetarian Nutrition. It was the first such course
on an American university campus and has been far more successful
than I could have imagined. The course focuses on the health value of a
plant-based diet. After spending my time at MIT and Virginia Tech, then
coming back to Cornell thirty years ago, I was charged with the task
of integrating the concepts and principles of chemistry, biochemistry,
physiology and toxicology in an upper-level course in nutrition.

After four decades of scientific research, education and policy making
at the highest levels in our society, I now feel I can adequately integrate
these disciplines into a cogent story. That's what I have done for my
most recent course, and many of my students tell me that their lives are
changed for the better by the end of the semester. That's what I intend
to do for you; I hope your life will be changed as well.

Part I

THE CHINA STUDY

. _ 1 _ _

Problems We Face,
Solutions We Need

"He who does not know food, how can he
understand the diseases of man?"

— Hippocrates, the father of medicine (460-357 B.C.)

On a golden morning in 1946, when summer was all tuckered out and
fall wanted to be let in, all you could hear on my family's dairy farm was
quiet. There was no growl from cars driving by or airplanes burning
trails overhead. Just quiet. There were the songbirds, of course, and the
cows, and the roosters who would chime in once in a while, but these
noises merely filled out the quiet, the peace.

Standing on the second floor of our barn, with the immense brown
doors gaping open, allowing the sun to soak through, I was a happy
twelve-year-old. I had just finished a big country breakfast of eggs, ba-
con, sausage, fried potatoes and ham with a couple of glasses of whole
milk. My mom had cooked a fantastic meal. I had been working up my
appetite since 4:30 a.m., when I had gotten up to milk the cows with my
father Tom and my brother Jack.

My father, then forty-five, stood with me in the quiet sun. He opened
a fifty-pound sack of alfalfa seed, dumped all the tiny seeds on the

1 1

THE CHINA STUDY

wooden barn floor in front of us and then opened a box containing fine
black powder. The powder, he explained, was bacteria that would help
the alfalfa grow They would attach themselves to the seeds and become
part of the roots of the growing plant throughout its life. Having had
only two years of formal education, my father was proud of knowing
that the bacteria helped the alfalfa convert nitrogen from the air into
protein. The protein, he explained, was good for the cows that would
eventually eat it. So our work that morning was to mix the bacteria and
the alfalfa seeds before planting. Always curious, I asked my dad why
it worked and how. He was glad to explain it, and I was glad to hear it.
This was important knowledge for a farm boy.

Seventeen years later, in 1963, my father had his first heart attack. He
was sixty-one. At age seventy, he died from a second massive coronary.
I was devastated. My father, who had stood with my siblings and me for
so many days in the quiet countryside, teaching us the things that I still
hold dear in life, was gone.

Now, after decades of doing experimental research on diet and health,
I know that the very disease that killed my father, heart disease, can be
prevented, even reversed. Vascular (arteries and heart) health is possible
without life-threatening surgery and without potentially lethal drugs. I
have learned that it can be achieved simply by eating the right food.

This is the story of how food can change our lives. I have spent my
career in research and teaching unraveling the complex mystery of why
health eludes some and embraces others, and I now know that food
primarily determines the outcome. This information could not come
at a better time. Our health care system costs too much, it excludes far
too many people and it does not promote health and prevent disease.
Volumes have been written on how the problem might be solved, but
progress has been painfully slow.

SICKNESS, ANYONE?

If you are male in this country, the American Cancer Society says that
you have a 47% chance of getting cancer. If you are female, you fare
a little better, but you still have a whopping 38% lifetime chance of
getting cancer. 1 The rates at which we die from cancer are among the
highest in the world, and it has been getting worse (Chart 1.1). Despite
thirty years of the massively funded War on Cancer, we have made little
progress.

Contrary to what many believe, cancer is not a natural event. Adopting

PROBLEMS WE FACE, SOLUTIONS WE NEED

CHART 1.1: CANCER DEATH RATES (PER 100,000 PEOPLE) 1

250

200

150

100

1972-1974

1992-1994

a healthy diet and lifestyle can prevent the majority of cancers in the
United States. Old age can and should be graceful and peaceful.

But cancer is only part of a larger picture of disease and death in
America. Looking elsewhere, we see that there is an overall pattern of
poor health. For example, we are rapidly becoming the heaviest people
on earth. Overweight Americans now significantly outnumber those
who maintain a healthy weight. As shown in Chart 1.2, our rates of
obesity have been skyrocketing over the past several decades. 2

According to the National Center for Health Statistics, almost a third
of the adults twenty years of age and over in this country are obese! 3
One is considered obese if he or she is carrying more than a third of a

CHART 1 .2: PERCENT OBESE POPULATION 2

1976-1980

1988-1994

1999-2000

THE CHINA STUDY

person above and beyond a healthy weight. Similarly frightening trends
have been occurring in children as young as two years of age. 3

CHART 1.3: WHAT IS OBESE (BOTH SEXES)?

Height

Weight in Excess of (lbs)

5'0"

153

5'2"

164

5'4"

174

5'6"

185

5'8"

197

5' 10"

209

6'0"

221

6'2"

233

But cancer and obesity are not the only epidemics casting a large
shadow over American health. Diabetes has also increased in unprec-
edented proportions. One out of thirteen Americans now has diabetes,
and that ratio continues to rise. If we don't heed the importance of diet,
millions of additional Americans will unknowingly develop diabetes
and suffer its consequences, including blindness, limb amputation,
cardiovascular disease, kidney disease and premature death. Despite
this, fast food restaurants that serve nutritionally defunct foods are now
fixtures in almost every town. We eat out more than ever 4 and speed
has taken precedence over quality. As we spend more time watching
TV, playing video games and using the computer, we are less physically
active.

Both diabetes and obesity are merely symptoms of poor health in gen-
eral. They rarely exist in isolation of other diseases and often forecast
deeper, more serious health problems, such as heart disease, cancer and
stroke. Two of the most frightening statistics show that diabetes among
people in their thirties has increased 70% in less than ten years and the
percentage of obese people has nearly doubled in the past thirty years.
Such an incredibly fast increase in these "signal" diseases in America's
young to middle-age population forecasts a health care catastrophe in
the coming decades. It may become an unbearable burden on a health
system that is already strained in countless ways.

PROBLEMS WE FACE, SOLUTIONS WE NEED 15

DIABETES STATISTICS
Percent Increase in Incidence from 1 990 to 1 998 s :

Age 30-39 (70%) • Age 40-49 (40%) • Age 50-59 (3 1 %)

Percent of Diabetics Who Aren't Aware of their Illness 3 : 34%

Diabetes Outcomes 6 : Heart Disease and Stroke; Blindness; Kidney Disease;
Nervous System Disorders; Dental Disease; Limb Amputation

Annual Economic Cost of Diabetes 7 : $98 Billion

But the most pervasive killer in our culture is not obesity, diabetes
or cancer. It is heart disease. Heart disease will kill one out of every
three Americans. According to the American Heart Association, over 60
million Americans currently suffer from some form of cardiovascular
disease, including high blood pressure, stroke and heart disease. 8 Like
me, you undoubtedly have known someone who died of heart disease.
But since my own father died from a heart attack over thirty years ago,
a great amount of knowledge has been uncovered in understanding this
disease. The most dramatic recent finding is that heart disease can be
prevented and even reversed by a healthy diet. 9 - 10 People who cannot
perform the most basic physical activity because of severe angina can
find a new life simply by changing their diets. By embracing this revo-
lutionary information, we could collectively defeat the most dangerous
disease in this country.

OOPS... WE DIDN'T MEAN TO HAVE THAT HAPPEN!

As increasing numbers of Americans fall victim to chronic diseases, we
hope that our hospitals and doctors will do all that they can to help us.
Unfortunately, both the newspapers and the courts are filled with stories
and cases that tell us that inadequate care has become the norm.

One of the most well regarded voices representing the medical
community, the Journal of the American Medical Association (JAMA),
included a recent article by Barbara Starfield, M.D., stating that physi-
cian error, medication error and adverse events from drugs or surgery
kill 225,400 people per year (Chart 1.5). 11 That makes our health care
system the third leading cause of death in the United States, behind only
cancer and heart disease (Chart 1.4). 12

16 THE CHINA STUDY

CHART 1.4: LEADING CAUSES OF DEATH 12

Cause of Death

Deaths

Diseases of the Heart

710,760

Cancer (Malignant Neoplasms)

553,091

Medical Care"

225,400

Stroke (Cerebrovascular Diseases]

167,661

Chronic Lower Respiratory Diseases

122,009

Accidents

97,900

Diabetes Mellitus

69,301

Influenza and Pneumonia

65,313

Alzheimer's Disease

49,558

CHART 1.5: DEATH BY HEALTH CARE"

Number of Americans Per Year Who Die From:

Medication Errors 13

7,400

Unnecessary Surgery 14

1 2,000

Other Preventable Errors in Hospitals 11

20,000

Hospital Borne Infections"

80,000

Adverse Drug Effects 15

1 06,000

The last and largest category of deaths in this group are the hospital-
ized patients who die from the "noxious, unintended and undesired ef-
fect of a drug," 15 which occurs at normal doses. 16 Even with the use of
approved medicines and correct medication procedures, over one hun-
dred thousand people die every year from unintended reactions to the
"medicine" that is supposed to be reviving their health. 15 Incidentally, this
same report, which summarized and analyzed thirty-nine separate stud-
ies, found that almost 7% (one out of fifteen) of all hospitalized patients
have experienced a serious adverse drug reaction, one that "requires hos-
pitalization, prolongs hospitalization, is permanendy disabling or results
in death." 15 These are people who took their medicine as directed. This
number does not include the tens of thousands of people who suffer from
the incorrect administration and use of these drugs. Nor does it include
adverse drug events that are labeled "possible" effects, or drugs that do

PROBLEMS WE FACE, SOLUTIONS WE NEED

not accomplish their intended goal. In other words, one of fifteen is a
conservative number. 15

If nutrition were better understood, and prevention and natural treat-
ments were more accepted in the medical community, we would not be
pouring so many toxic, potentially lethal drugs into our bodies at the
last stage of disease. We would not be frantically searching for the new
medicine that alleviates the symptoms but often does nothing to address
the fundamental causes of our illnesses. We would not be spending our
money developing, patenting and commercializing "magic bullet" drugs
that often cause additional health problems. The current system has not
lived up to its promise. It is time to shift our thinking toward a broader
perspective on health, one that includes a proper understanding and
use of good nutrition.

As I look back on what I've learned, I am appalled that the circum-
stances surrounding the way in which Americans die are often unneces-
sarily early painful and costly.

AN EXPENSIVE GRAVE

We pay more for our health care than any other country in the world
(Chart 1.6).

We spent over a trillion dollars on health care in 1997. 17 In fact, the
cost of our "health" is spiraling so far out of control that the Health
Care Financing Administration predicted that our system would cost 16
trillion dollars by 2030. 17 Costs have so consistently outpaced inflation
that we now spend one out of every seven dollars the economy pro-
duces on health care (Chart 1.7). We have seen almost a 300% increase
in expenditures, as a percentage of GDP, in less than forty years! What is
all the extra financing buying? Is it creating health? I say no, and many
serious commentators agree.

Recently the health status of twelve countries including the U.S.,
Canada, Australia and several Western European countries was com-
pared on the basis of sixteen different indicators of health care efficacy. 19
Other countries spend, on average, only about one-half of what the U.S.
spends per capita on health care. Isn't it reasonable, therefore, for us to
expect our system to rank above theirs? Unfortunately, among these
twelve countries, the U.S. system is consistently among the worst per-
formers. 11 In a separate analysis, the World Health Organization ranked
the United States thirty-seventh best in the world according to health
care system performance. 20 Our health care system is clearly not the best

THE CHINA STUDY

CHART 1.6: HEALTH CARE EXPENDITURES PER PERSON, 1997 $US 17

3912

4000

CHART 1.7: PERCENT OF U.S. GDP SPENT ON HEALTH CARE 17 ' 18

1960

1970

1980

1990

1997

in the world, even though we spend, far and away, the most money on
it.

Too often in the United States, a doctor's treatment decisions are
made on the basis of money, not health. The consequences of not hav-
ing health insurance, I suspect, have never been more terrifying, and
close to 44 million Americans are uninsured. 21 It's unacceptable to me

PROBLEMS WE FACE, SOLUTIONS WE NEED

that we spend more money on health care than any other country on
this planet, and we still have tens of millions of people without access
to basic care.

From three perspectives — disease prevalence, medical care efficacy
and economics — we have a deeply troubled medical system. But I do
not do justice to this topic simply by recounting figures and statistics.
Many of us have spent awful times in hospitals or in nursing homes
watching a loved one succumb to disease. Perhaps you've been a patient
yourself and you know firsthand how poorly the system sometimes
functions. Isn't it paradoxical that the system that is supposed to heal us
too often hurts us?

WORKING TO LESSEN CONFUSION

The American people need to know the truth. They need to know what
we have uncovered in our research. People need to know why we are
unnecessarily sick, why too many of us die early despite the billions
spent on research. The irony is that the solution is simple and inexpen-
sive. The answer to the American health crisis is the food that each of us
chooses to put in our mouths each day. It's as simple as that.

Although many of us think we're well informed on nutrition, we're
not. We tend to follow one faddish diet after another. We disdain satu-
rated fats, butter or carbohydrates, and then embrace vitamin E, calcium
supplements, aspirin or zinc and focus our energy and effort on extreme-
ly specific food components, as if this will unlock the secrets of health.
All too often, fancy outweighs fact. Perhaps you remember the protein
diet fad that gripped the country in the late 1970s. The promise was that
you could lose weight by replacing real food with a protein shake. In a
very short while, almost sixty women died from the diet. More recently
millions have adopted high-protein, high-fat diets based on books such
as Dr. Atkins' New Diet Revolution, Protein Power and The South Beach
Diet. There is increasing evidence that these modern protein fads contin-
ue to inflict a great variety of dangerous health disorders. What we don't
know — what we don't understand — about nutrition can hurt us.

I've been wrestling with this public confusion for more than two de-
cades. In 1988, 1 was invited before the U.S. Senate Governmental Affairs
Committee, chaired by Senator John Glenn, to give my views on why the
public is so confused about diet and nutrition. After examining this issue
both before and since that testimony, I can confidendy state that one of
the major sources of confusion is this: far too often, we scientists focus on

THE CHINA STUDY

details while ignoring the larger context. For example, we pin our efforts
and our hopes on one isolated nutrient at a time, whether it is vitamin A to
prevent cancer or vitamin E to prevent heart attacks. We oversimplify and
disregard the infinite complexity of nature. Often, investigating minute bio-
chemical parts of food and trying to reach broad conclusions about diet and
health leads to contradictory results. Contradictory results lead to confused
scientists and policy makers, and to an increasingly confused public.

A DIFFERENT KIND OF PRESCRIPTION

Most of the authors of several best-selling "nutrition" books claim to be
researchers, but I am not aware that their "research" involves original,
professionally developed experimentation. That is, they have not de-
signed and conducted studies under the scrutiny of fellow colleagues or
peers. They have few or no publications in peer-reviewed scientific jour-
nals; they have virtually no formal training in nutritional science; they
belong to no professional research societies; they have not participated
as peer reviewers. They do, nonetheless, often develop very lucrative
projects and products that put money in their pockets while leaving the
reader with yet another short-lived and useless diet fad.

If you are familiar with the "health" books at your nearby bookstore,
you have likely heard of Dr. Atkins' New Diet Revolution, The South Beach
Diet, Sugar Busters, The Zone or Eat Right for Your Type. These books
have made health information more confusing, more difficult to grasp
and ultimately more elusive. If you aren't fatigued, constipated or half-
starved by these quick-fix plans, your head is spinning from counting
calories and measuring grams of carbohydrates, protein and fat. What's
the real problem, anyway? Is it fat? Is it carbohydrates? What's the ratio
of nutrients that provides greatest weight loss? Are cruciferous vegeta-
bles good for my blood type? Am I taking the right supplements? How
much vitamin C do I need every day? Am I in ketosis? How many grams
of protein do I need?

You get the picture. This is not health. These are fad diets that em-
body the worst of medicine, science and the popular media.

If you are only interested in a two-week menu plan to lose weight,
then this book is not for you. I am appealing to your intelligence, not to
your ability to follow a recipe or menu plan. I want to offer you a more
profound and more beneficial way to view health. I have a prescrip-
tion for maximum health that is simple, easy to follow and offers more
benefits than any drug or surgery, without any of the side effects. This

PROBLEMS WE FACE, SOLUTIONS WE NEED

prescription isn't merely a menu plan; it doesn't require daily charts or
calorie counting; and it doesn't exist to serve my own financial inter-
ests. Most importantly, the supporting evidence is overwhelming. This
is about changing the way you eat and live and the extraordinary health
that will result.

So, what is my prescription for good health? In short, it is about
the multiple health benefits of consuming plant-based foods, and the
largely unappreciated health dangers of consuming animal-based foods,
including all types of meat, dairy and eggs. I did not begin with pre-
conceived ideas, philosophical or otherwise, to prove the worthiness
of plant-based diets. I started at the opposite end of the spectrum: as
a meat-loving dairy farmer in my personal life and an "establishment"
scientist in my professional life. I even used to lament the views of veg-
etarians as I taught nutritional biochemistry to pre-med students.

My only interest now is to explain the scientific basis for my views
in the clearest way possible. Changing dietary practices will only occur
and be maintained when people believe the evidence and experience
the benefits. People decide what to eat for a number of reasons, health
considerations being only one. My task is only to present the scientific
evidence in a form that can be understood. The rest is up to you.

The scientific basis for my views is largely empirical, obtained
through observation and measurement. It is not illusory, hypothetical
or anecdotal; it is from legitimate research findings. It is a type of sci-
ence originally advocated 2,400 years ago by the Father of Medicine,
Hippocrates, who said, "There are, in effect, two things: to know and to
believe one knows. To know is science. To believe one knows is igno-
rance." I plan to show you what I have come to know.

Much of my evidence comes from human studies done by myself and
by my students and colleagues in my research group. These studies were
diverse both in design and in purpose. They included an investigation
of liver cancer in Philippine children and their consumption of a mold
toxin, anatoxin 22 ' 23 ; a nationwide program of self-help nutrition centers
for malnourished preschool children in the Philippines 24 ; a study of
dietary factors affecting bone density and osteoporosis in 800 women
in China 25-27 ; a study of biomarkers that characterize the emergence of
breast cancer 28, 29 ; and a nationwide, comprehensive study of dietary
and lifestyle factors associated with disease mortality in 170 villages in
mainland China and Taiwan (widely known as the China Study). 30-33

These studies, exceptionally diverse in scope, dealt with diseases

THE CHINA STUDY

thought to be related to varied dietary practices, thus providing the op-
portunity to investigate diet and disease associations comprehensively.
The China Study, of which I was director, began in 1983 and is still
ongoing.

In addition to these human studies, I maintained a twenty-seven-year
laboratory research program in experimental animal studies. Begun in
the late 1960s, this National Institutes of Health (NIH)-funded research
investigated the link between diet and cancer in considerable depth.
Our findings, which were published in the highest quality scientific
journals, brought into question the very core principles of cancer cau-
sation.

When all was said and done, my colleagues and I were honored to
have received a total of seventy-four grant-years of funding. In other
words, because we had more than one research program being con-
ducted at once, my colleagues and I did seventy-four years' worth of
funded research in less than thirty-five years. From this research I have
authored or co-authored over 350 scientific articles. Numerous awards
were extended to me and to my students and colleagues for this long
series of studies and publications. They included, among others, the
1998 American Institute for Cancer Research award "in recognition
of a lifetime of significant accomplishments in scientific research ... in
diet, nutrition and cancer," a 1998 award as one of the "Top 25 Food
Influentials" by Self magazine and the 2004 Burton Kallman Scientific
Award by the Natural Nutrition Food Association. Moreover, invitations
to lecture at research and medical institutions in more than forty states
and several foreign countries attested to the interest in these findings
from the professional communities. My appearance before congressio-
nal committees and federal and state agencies also indicated substantial
public interest in our findings. Interviews on the McNeil-Lehrer News
Hour program, at least twenty-five other TV programs, lead stories in
USA Today, the New York Times, and the Saturday Evening Post and
widely publicized TV documentaries on our work have also been a part
of our public activities.

THE PROMISE OF THE FUTURE

Through all of this, I have come to see that the benefits produced by eat-
ing a plant-based diet are far more diverse and impressive than any drug
or surgery used in medical practice. Heart diseases, cancers, diabetes,
stroke and hypertension, arthritis, cataracts, Alzheimer's disease, impo-

PROBLEMS WE FACE, SOLUTIONS WE NEED

tence and all sorts of other chronic diseases can be largely prevented.
These diseases, which generally occur with aging and tissue degenera-
tion, kill the majority of us before our time.

Additionally, impressive evidence now exists to show that advanced
heart disease, relatively advanced cancers of certain types, diabetes and
a few other degenerative diseases can be reversed by diet. I remember
when my superiors were only reluctantly accepting the evidence of nu-
trition being able to prevent heart disease, for example, but vehemently
denying its ability to reverse such a disease when already advanced. But
the evidence can no longer be ignored. Those in science or medicine
who shut their minds to such an idea are being more than stubborn;
they are being irresponsible.

One of the more exciting benefits of good nutrition is the prevention
of diseases that are thought to be due to genetic predisposition. We now
know that we can largely avoid these "genetic" diseases even though we
may harbor the gene (or genes) that is (are) responsible for the disease.
But funding of genetic research continues to spiral upwards in the belief
that specific genes account for the occurrence of specific diseases, in
the hope that we somehow will be able to "turn off these nasty genes.
Drug company public relations programs now depict a future where
each of us will have a personal ID card cataloging all of our good and
bad genes. Using this card, we will be expected to go to our doctor, who
will prescribe a single pill to suppress our bad genes. I strongly suspect
these miracles will never be realized, or if tried they will have serious,
unintended consequences. These futuristic pipe dreams obscure the
affordable, efficacious health solutions that currently exist: solutions
based in nutrition.

In my own laboratory we have shown in experimental animals that
cancer growth can be turned on and off by nutrition, despite very strong
genetic predisposition. We have studied these effects in great detail and
have published our findings in the very best scientific journals. As you
will see later, these findings are nothing short of spectacular, and the
same effects have been indicated over and over again in humans.

Eating the right way not only prevents disease but also generates
health and a sense of well-being, both physically and mentally Some
world-class athletes, such as ironman Dave Scott, track stars Carl
Lewis and Edwin Moses, tennis great Martina Navratilova, world cham-
pion wrestler Chris Campbell (no relation) and sixty-eight-year-old
marathoner Ruth Heidrich have discovered that consuming a low-fat,

THE CHINA STUDY

plant-based diet gives them a significant edge in performance. In the
laboratory, we fed experimental rats a diet similar to the usual American
fare — rich in animal-based protein — and compared them with other
rats fed a diet low in animal-based protein. Guess what happened when
both sets of rats had an opportunity to voluntarily use exercise wheels?
Those fed the low-animal protein diet exercised substantially more,
with less fatigue, than those fed the type of diet that most of us eat. This
was the same effect observed by these world-class athletes.

This shouldn't be news to the medical establishment. A century ago,
Professor Russell Chittenden, a famous, well established nutrition re-
searcher at Yale University Medical School, investigated whether eating
a plant-based diet affected students' physical capacities. 34,35 He fed some
students, fellow faculty and himself a plant-based diet and measured
their physical performance tests. He got the same results as our rats
almost a century later — and they were equally spectacular.

Then there is the question of our excessive dependence on drugs and
surgery to control our health. In its simplest form, eating the right way
would largely obviate the enormous costs of using drugs, as well as their
side effects. Fewer people would need to wage lengthy, expensive battles
with chronic disease in hospitals over their last years of life. Health care
costs would drop and medical mistakes would wane as premature death
plummeted. In essence, our health care system would finally protect
and promote our health as it is meant to do.

SIMPLE BEGINNINGS

As I look back, I often think about life on the farm and how it shaped
my thinking in so many ways. My family was immersed in nature every
waking moment. In the summer, from sunrise to sunset, we were out-
doors planting and harvesting the crops and taking care of the animals.
My mother had the best garden in our part of the country and toiled day
in and day out during the summer to keep our family well fed with fresh
food, all produced on our own farm.

I've had an amazing journey, to be sure. I have been startled time and
time again by what I have learned. I wish that my family and others
around us had had the same information back in the mid-1900s that
we now have about food and health. If we had, my father could have
prevented, or reversed, his heart disease. He could have met my young-
est son, his namesake, who is collaborating with me on this book. He
might have lived for several more years with a higher quality of health.

PROBLEMS WE FACE, SOLUTIONS WE NEED

My journey in science over the past forty-five years has convinced me
that it is now more urgent than ever to show how people can avoid these
tragedies. The science is there and it must be made known. We cannot
let the status quo go unchallenged and watch our loved ones suffer un-
necessarily. It is time to stand up, clear the air and take control of our
health.

_ 2 _

A House of Proteins

My entire professional career in biomedical research has centered on
protein. Like an invisible leash, protein tethered me wherever I went,
from the basic research laboratory to the practical programs of feeding
malnourished children in the Philippines to the government board-
rooms where our national health policy was being formulated. Protein,
often regarded with unsurpassed awe, is the common thread tying to-
gether past and present knowledge about nutrition.

The story of protein is part science, part culture and a good dose of
mythology. I am reminded of the words of Goethe, first brought to my
attention by my friend Howard Lyman, a prominent lecturer, author
and former cattle rancher: "We are best at hiding those things which
are in plain sight." Nothing has been so well hidden as the untold story
of protein. The dogma surrounding protein censures, reproaches and
guides, directly or indirectly, almost every thought we have in biomedi-
cal research.

Ever since the discovery of this nitrogen-containing chemical in 1839
by the Dutch chemist Gerhard Mulder, protein has loomed as the most
sacred of all nutrients. The word protein comes from the Greek word
proteios, which means "of prime importance."

In the nineteenth century, protein was synonymous with meat, and
this connection has stayed with us for well over a hundred years. Many
people today still equate protein with animal-based food. If you were to
name the first food that comes to mind when 1 say protein, you might
say beef. If you did, you aren't alone.

THE CHINA STUDY

Confusion reigns on many of the most basic questions about protein:

• What are good sources of protein?

• How much protein should one consume?

• Is plant protein as good as animal protein?

• Is it necessary to combine certain plant foods in a meal to get com-
plete proteins?

• Is it advisable to take protein powders or amino acid supplements,
especially for someone who does vigorous exercise or plays sport?

• Should one take protein supplements to build muscle?

• Some protein is considered high quality, some low quality; what
does this mean?

• Where do vegetarians get protein?

• Can vegetarian children grow properly without animal protein?

Fundamental to many of these common questions and concerns is
the belief that meat is protein and protein is meat. This belief comes
from the fact that the "soul" of animal-based foods is protein. In many
meat and dairy products, we can selectively remove the fat but we are
still left with recognizable meat and dairy products. We do this all the
time, with lean cuts of meat and skim milk. But if we selectively remove
the protein from animal-based foods, we are left with nothing like the
original. A non-protein steak, for example, would be a puddle of water,
fat and a small amount of vitamins and minerals. Who would eat that?
In brief, for a food to be recognized as an animal-based food, it must
have protein. Protein is the core element of animal-based foods.

Early scientists like Carl Voit (1831-1908), a prominent German
scientist, were staunch champions of protein. Voit found that "man"
needed only 48.5 grams per day, but nonetheless he recommended a
whopping 118 grams per day because of the cultural bias of the time.
Protein equaled meat, and everyone aspired to have meat on his or her
table, just as we aspire to have bigger houses and faster cars. Voit figured
you can't get too much of a good thing.

Voit went on to mentor several well-known nutrition researchers of
the early 1900s, including Max Rubner (1854-1932) and WO. Atwater
(1844-1907). Both students closely followed the advice of their teacher.
Rubner stated that protein intake, meaning meat, was a symbol of civi-
lization itself: "a large protein allowance is the right of civilized man."
Atwater went on to organize the first nutrition laboratory at the United
States Department of Agriculture (USDA). As director of the USDA, he

A HOUSE OF PROTEINS

recommended 125 grams per day (only about fifty-five grams per day is
now recommended). Later, we will see how important this early prec-
edent was to this government agency.

A cultural bias had become firmly entrenched. If you were civilized,
you ate plenty of protein. If you were rich, you ate meat, and if you were
poor, you ate staple plant foods, like potatoes and bread. The lower
classes were considered by some to be lazy and inept as a result of not
eating enough meat, or protein. Elitism and arrogance dominated much
of the burgeoning field of nutrition in the nineteenth century. The en-
tire concept that bigger is better, more civilized and perhaps even more
spiritual permeated every thought about protein.

Major McCay, a prominent English physician in the early twentieth
century, provided one of the more entertaining, but most unfortunate,
moments in this history. Physician McCay was stationed in the English
colony of India in 1912 in order to identify good fighting men in the In-
dian tribes. Among other things, he said that people who consumed less
protein were of a "poor physique, and a cringing effeminate disposition
is all that can be expected."

PRESSING FOR QUALITY

Protein, fat, carbohydrate and alcohol provide virtually all of the calo-
ries that we consume. Fat, carbohydrate and protein, as macronutrients,
make up almost all the weight of food, aside from water, with the re-
maining small amount being the vitamin and mineral micronutrients.
The amounts of these latter micronutrients needed for optimum health
are tiny (milligrams to micrograms).

Protein, the most sacred of all nutrients, is a vital component of our
bodies and there are hundreds of thousands of different kinds. They
function as enzymes, hormones, structural tissue and transport mol-
ecules, all of which make life possible. Proteins are constructed as long
chains of hundreds or thousands of amino acids, of which there are
fifteen to twenty different kinds, depending on how they are counted.
Proteins wear out on a regular basis and must be replaced. This is ac-
complished by consuming foods that contain protein. When digested,
these proteins give us a whole new supply of amino acid building blocks
to use in making new protein replacements for those that wore out.
Various food proteins are said to be of different quality, depending on
how well they provide the needed amino acids used to replace our body
proteins.

THE CHINA STUDY

This process of disassembling and reassembling the amino acids of
proteins is like someone giving us a multicolored string of beads to re-
place an old string of beads that we lost. However, the colored beads on
the string given to us are not in the same order as the string we lost. So,
we break the string and collect its beads. Then, we reconstruct our new
string so that the colored beads are in the same order as our lost string.
But if we are short of blue beads, for example, making our new string is
going to be slowed down or stopped until we get more blue beads. This
is the same concept as in making new tissue proteins to match our old
worn out proteins.

About eight amino acids ("colored beads") that are needed for mak-
ing our tissue proteins must be provided by the food we eat. They are
called "essential" because our bodies cannot make them. If, like our
string of beads, our food protein lacks enough of even one of these
eight "essential" amino acids, then the synthesis of the new proteins
will be slowed down or stopped. This is where the idea of protein qual-
ity comes into play. Food proteins of the highest quality are, very sim-
ply, those that provide, upon digestion, the right kinds and amounts of
amino acids needed to efficiently synthesize our new tissue proteins.
This is what that word "quality" really means: it is the ability of food
proteins to provide the right kinds and amounts of amino acids to make
our new proteins.

Can you guess what food we might eat to most efficiently provide
the building blocks for our replacement proteins? The answer is human
flesh. Its protein has just the right amount of the needed amino acids.
But while our fellow men and women are not for dinner, we do get
the next "best" protein by eating other animals. The proteins of other
animals are very similar to our proteins because they mostly have the
right amounts of each of the needed amino acids. These proteins can be
used very efficiently and therefore are called "high quality" Among ani-
mal foods, the proteins of milk and eggs represent the best amino acid
matches for our proteins, and thus are considered the highest quality.
While the "lower quality" plant proteins may be lacking in one or more
of the essential amino acids, as a group they do contain all of them.

The concept of quality really means the efficiency with which food
proteins are used to promote growth. This would be well and good if the
greatest efficiency equaled the greatest health, but it doesn't, and that's
why the terms efficiency and quality are misleading. In fact, to give you
a taste of what's to come, there is a mountain of compelling research

A HOUSE OF PROTEINS

showing that "low-quality" plant protein, which allows for slow but
steady synthesis of new proteins, is the healthiest type of protein. Slow
but steady wins the race. The quality of protein found in a specific food
is determined by seeing how fast animals would grow while consuming
it. Some foods, namely those from animals, emerge with a very high
protein efficiency ratio and value. 1

This focus on efficiency of body growth, as if it were good health, en-
courages the consumption of protein with the highest "quality." As any
marketer will tell you, a product that is defined as being high quality
instantly earns the trust of consumers. For well over 100 years, we have
been captive to this misleading language and have oftentimes made the
unfortunate leap to thinking that more quality equals more health.

The basis for this concept of protein quality was not well known
among the public, but its impact was — and still is — highly significant.
People, for example, who choose to consume a plant-based diet will
often ask, even today, "Where do I get my protein?" as if plants don't
have protein. Even if it is known that plants have protein, there is still
the concern about its perceived poor quality. This has led people to
believe that they must meticulously combine proteins from different
plant sources during each meal so that they can mutually compensate
for each other's amino acid deficits. However, this is overstating the
case. We now know that through enormously complex metabolic sys-
tems, the human body can derive all the essential amino acids from the
natural variety of plant proteins that we encounter every day. It doesn't
require eating higher quantities of plant protein or meticulously plan-
ning every meal. Unfortunately, the enduring concept of protein quality
has greatly obscured this information.

THE PROTEIN GAP

The most important issue in nutrition and agriculture during my early
career was figuring out ways to increase the consumption of protein,
making sure it was of the highest possible quality. My colleagues and I
all believed in this common goal. From my early years on the farm to my
graduate education, I accepted this virtual reverence for protein. As a
youngster, I remember that the most expensive part of farm animal feed
was the protein supplements that we fed to our cows and pigs. Then,
at graduate school, I spent three years (1958-1961) doing my Ph.D. re-
search trying to improve the supply of high-quality protein by growing
cows and sheep more efficiently so we could eat more of them. 2 3

THE CHINA STUDY

I went all the way through my graduate studies with a profound be-
lief that promoting high-quality protein, as in animal-based foods, was
a very important task. My graduate research, although cited a few times
over the next decade or so, was only a small part of much larger efforts
by other research groups to address a protein situation worldwide. Dur-
ing the 1960s and 1970s, I was to hear over and over again about a so-
called "protein gap" in the developing world." 1

The protein gap stipulated that world hunger and malnutrition
among children in the third world was a result of not having enough
protein to consume, especially high-quality (i.e. animal) protein. 1, 4,5
According to this view, those in the third world were especially de-
ficient in "high-quality" protein, or animal protein. Projects were
springing up all over the place to address this "protein gap" problem.
A prominent MIT professor and his younger colleague concluded in
1976 that "an adequate supply of protein is a central aspect of the world
food problem" 3 and further that "unless . . . desirably [supplemented]
by modest amounts of milk, eggs, meat or fish, the predominantly
cereal diets [of poor nations] are . . . deficient in protein for growing chil-
dren "To address this dire problem:

• MIT was developing a protein-rich food supplement called INCA-
PARINA.

• Purdue University was breeding corn to contain more lysine, the
"deficient" amino acid in corn protein.

• The U.S. government was subsidizing the production of dried milk
powder to provide high-quality protein for the world's poor.

• Cornell University was providing a wealth of talent to the Philip-
pines to help develop both a high-protein rice variety and a live-
stock industry.

• Auburn University and MIT were grinding up fish to produce "fish
protein concentrate" to feed the world's poor.

The United Nations, the U.S. Government Food for Peace Program,
major universities and countless other organizations and universities
were taking up the battle cry to eradicate world hunger with high-qual-
ity protein. I knew most of the projects firsthand, as well as the indi-
viduals who organized and directed them.

The Food and Agriculture Organization (FAO) of the United Nations
exerts considerable influence in developing countries through their ag-
riculture development programs. Two of its staffers 6 declared in 1970

A HOUSE OF PROTEINS

that ". . .by and large, the lack of protein is without question the most
serious qualitative deficiency in the nutrition of developing countries.
The great mass of the population of these countries subsists mainly on
foods derived from plants frequently deficient in protein, which results
in poor health and low productivity per man." M. Autret, a very influ-
ential man from the FAO, added that "owing to the low-animal protein
content of the diet and lack of diversity of supplies [in developing
countries], protein quality is unsatisfactory." 4 He reported on a very
strong association between consumption of animal-based foods and an-
nual income. Autret strongly advocated increasing the production and
consumption of animal protein in order to meet the growing "protein
gap" in the world. He also advocated that "all resources of science and
technology must be mobilized to create new protein-rich foods or to
derive the utmost benefits from hitherto insufficiently utilized resources
to feed mankind." 4

Bruce Stillings at the University of Maryland and the U.S. Depart-
ment of Commerce, another proponent of consuming animal-based di-
ets, admitted in 1973 that "although there is no requirement for animal
protein in the diet per se, the quantity of dietary protein from animal
sources is usually accepted as being indicative of the overall protein
quality of the diet." 1 He went on to say that the " . . .supply of adequate
quantities of animal products is generally recognized as being an ideal
way to improve world protein nutrition."

Of course, it's quite correct that a supply of protein can be an im-
portant way of improving nutrition in the third world, particularly if
populations are getting all of their calories from one plant source. But
it's not the only way, and, as we shall see, it isn't necessarily the way
most consistent with long-term health.

FEEDING THE CHILDREN

So this was the climate at that time, and I was a part of it as much as
anyone else. I left MIT to take a faculty position at Virginia Tech in 1965.
Professor Charlie Engel, who was then the head of the Department of
Biochemistry and Nutrition at Virginia Tech, had considerable inter-
est in developing an international nutrition program for malnourished
children. He was interested in implementing a "mothercraft" self-help
project in the Philippines. This project was called "mothercraft" because
it focused on educating mothers of malnourished children. The idea was
that if mothers were taught that the right kinds of locally grown foods can

THE CHINA STUDY

make their children well, they would not have to rely on scarce medicines
and the mostly nonexistent doctors. Engel started the program in 1967
and invited me to be his Campus Coordinator and to come for extended
stays in the Philippines while he resided full time in Manila.

Consistent with the emphasis on protein as a means of solving mal-
nutrition, we had to make this nutrient the centerpiece of our educa-
tional "mothercraft" centers and thereby help to increase protein con-
sumption. Fish as a source of protein was mostly limited to the seacoast
areas. Our own preference was to develop peanuts as a source of protein
because this was a crop that could be grown most anywhere. The peanut
is a legume, like alfalfa, soybeans, clover, peas and other beans. Like
these other nitrogen "fixers," peanuts are rich in protein.

There was, however, a nagging problem with these tasty legumes.
Considerable evidence had been emerging, first from England 7 " 9 and
later from MIT (the same lab that I had worked in) 10 ' 11 to show that pea-
nuts often were contaminated with a fungus-produced toxin called af-
la toxin (AF). It was an alarming problem because AF was being shown
to cause liver cancer in rats. It was said to be the most potent chemical
carcinogen ever discovered.

So we had to tackle two closely related projects: alleviate childhood
malnutrition and resolve the AF contamination problem.

Prior to going to the Philippines, I had traveled to Haiti in order to
observe a few experimental mothercraft centers organized by my col-
leagues at Virginia Tech, Professors Ken King and Ryland Webb. It was
my first trip to an underdeveloped country, and Haiti certainly fit the
bill. Papa Doc Duvalier, president of Haiti, extracted what little resourc-
es the country had for his own rich lifestyle. In Haiti at that time 54%
of the children were dead before reaching their fifth birthday, largely
because of malnutrition.

I subsequently went to the Philippines and encountered more of the
same. We decided where mothercraft centers were to be located based
on how much malnutrition was present in each village. We focused our
efforts on the villages in most need. In a preliminary survey in each vil-
lage (barrio), children were weighed and their weight for age was com-
pared with a Western reference standard, which was subdivided into
first, second and third degree malnutrition. Third degree malnutrition,
the worst kind, represented children under the 65 th percentile. Keep in
mind that a child at the 100 th percentile represents only the average for
the U.S. Being less than the 65 ,h percentile means near starvation.

A HOUSE OF PROTEINS

In the urban areas of some of the big cities, as many as 15-20% of
the children aged three to six years were judged to be third degree. I
can so well remember some of my initial observations of these children.
A mother, hardly more than a wisp herself, holding her three-year-old
twins with bulging eyes, one at eleven pounds, the other at fourteen
pounds, trying to get them to open their mouths to eat some porridge.
Older children blind from malnutrition, being led around by their
younger siblings to seek a handout. Children without legs or arms hop-
ing to get a morsel of food.

A REVELATION TO DIE FOR

Needless to say, those sights gave us ample motivation to press ahead
with our project. As I mentioned before, we first had to resolve the
problem of AF contamination in peanuts, our preferred protein food.

The first step of investigating AF was to gather some basic information.
Who in the Philippines was consuming AF, and who was subject to liver
cancer? To answer these questions, I applied for and received a National
Institutes of Health (NIH) research grant. We also adopted a second strat-
egy by asking another question: how does AF actually affect liver cancer?
We wanted to study this question at the molecular level using laboratory
rats. I succeeded in getting a second NIH grant for this in-depth bio-
chemical research. These two grants initiated a two-track research inves-
tigation, one basic and one applied, which was to continue for the rest of
my career. I found studying questions both from the basic and applied
perspectives rewarding because it tells us not only the impact of a food
or chemical on health, but also why it has that impact. In so doing, we
could better understand not only the biochemical foundation of food and
health, but also how it might relate to people in everyday life.

We began with a stepwise series of surveys. First, we wanted to know
which foods contained the most AF We learned that peanuts and corn
were the foods most contaminated. All twenty-nine jars of peanut butter
we had purchased in the local groceries, for example, were contami-
nated, with levels of AF as much as 300 times the amount judged to be
acceptable in U.S. food. Whole peanuts were much less contaminated;
none exceeded the AF amounts allowed in U.S. commodities. This
disparity between peanut butter and whole peanuts originated at the
peanut factory. The best peanuts, which filled "cocktail" jars, were hand
selected from a moving conveyor belt, leaving the worst, moldiest nuts
to be delivered to the end of the belt to make peanut butter.

THE CHINA STUDY

Our second question concerned who was most susceptible to this AF
contamination and its cancer-producing effects. We learned that it was
children. They were the ones consuming the AF-laced peanut butter.
We estimated AF consumption by analyzing the excretion of AF meta-
bolic products in the urine of children living in homes with a partially
consumed peanut butter jar. 12 As we gathered this information an inter-
esting pattern emerged: the two areas of the country with the highest
rates of liver cancer, the cities of Manila and Cebu, also were the same
areas where the most AF was being consumed. Peanut butter was almost
exclusively consumed in the Manila area while corn was consumed in
Cebu, the second most populated city in the Philippines.

But, as it turned out, there was more to this story. It emerged from my
making the acquaintance of a prominent doctor, Dr. Jose Caedo, who
was an advisor to President Marcos. He told me that the liver cancer
problem in the Philippines was quite serious. What was so devastating
was that the disease was claiming the lives of children before the age of
ten. Whereas in the West, this disease mostly strikes people only after
forty years of age, Caedo told me that he had personally operated on
children younger than four years of age for liver cancer!

That alone was incredible, but what he then told me was even more
striking. Namely, the children who got liver cancer were from the best-fed
families. The families with the most money ate what we thought were
the healthiest diets, the diets most like our own meaty American diets.
They consumed more protein than anyone else in the country (high quality
animal protein, at that), and yet they were the ones getting liver cancer!

How could this be? Worldwide, liver cancer rates were highest in
countries with the lowest average protein intake. It was therefore widely
believed that this cancer was the result of a deficiency in protein. Fur-
ther, the deficiency problem was a major reason we were working in the
Philippines: to increase the consumption of protein by as many mal-
nourished children as possible. But now Dr. Caedo and his colleagues
were telling me that the most protein-rich children had the highest rates
of liver cancer. This seemed strange to me, at first, but over time my
own information increasingly confirmed their observations.

At that time, a research paper from India surfaced in an obscure med-
ical journal. 13 It was an experiment involving liver cancer and protein
consumption in two groups of laboratory rats. One group was given AF
and then fed diets containing 20% protein. The second group was given
the same level of AF and then fed diets containing only 5% protein.

A HOUSE OF PROTEINS

Every single rat fed 20% protein got liver cancer or its precursor lesions,
but not a single animal fed a 5% protein diet got liver cancer or its pre-
cursor lesions. It was not a trivial difference; it was 100% versus 0%.
This was very much consistent with my observations for the Philippine
children. Those who were most vulnerable to liver cancer were those
who consumed diets higher in protein.

No one seemed to accept the report from India. On a flight from De-
troit after returning from a presentation at a conference, I traveled with
a former but much senior colleague of mine from MIT, Professor Paul
Newberne. At the time, Newberne was one of the only people who had
given much thought to the role of nutrition in the development of can-
cer. I told him about my impressions in the Philippines and the paper
from India. He summarily dismissed the paper by saying, "They must
have gotten the numbers on the animal cages reversed. In no way could
a high-protein diet increase the development of cancer."

I realized that I had encountered a provocative idea that stimulated
disbelief, even the ire of fellow colleagues. Should I take seriously the
observation that protein increased cancer development and run the risk
of being thought a fool? Or should I turn my back on this story?

In some ways it seemed that this moment in my career had been fore-
shadowed by events in my personal life. When I was five years old, my
aunt who was living with us was dying of cancer. On several occasions
my uncle took my brother Jack and me to see his wife in the hospital.
Although I was too young to understand everything that was happen-
ing, I do remember being struck by the big "C" word: cancer. I would
think, "When I get big, I want to find a cure for cancer."

Many years later, just a few years after getting married, at about the
time when I was starting my work in the Philippines, my wife's mother
was dying of colon cancer at the young age of fifty-one. At that time, I
was becoming aware of a possible diet-cancer connection in our early
research. Her case was particularly difficult because she did not receive
appropriate medical care due to the fact that she did not have health
insurance. My wife Karen was her only daughter and they had a very
close relationship. These difficult experiences were making my career
choice easy: I would go wherever our research led me to help get a bet-
ter understanding of this horrific disease.

Looking back on it, this was the beginning of my career focus on diet
and cancer. The moment of deciding to investigate protein and cancer
was the turning point. If I wanted to stay with this story there was only

THE CHINA STUDY

one solution: start doing fundamental laboratory research to see not only
if, but also how, consuming more protein leads to more cancer. That's
exactly what I did. It took me farther than I had ever imagined. The ex-
traordinary findings my colleagues, students and I generated just might
make you think twice about your current diet. But even more than that,
the findings led to broader questions, questions that would eventually
lead to cracks in the very foundations of nutrition and health.

THE NATURE OF SCIENCE— WHAT YOU NEED TO KNOW
TO FOLLOW THE RESEARCH

Proof in science is elusive. Even more than in the "core" sciences of biol-
ogy, chemistry and physics, establishing absolute proof in medicine and
health is nearly impossible. The primary objective of research investiga-
tion is to determine only what is likely to be true. This is because research
into health is inherently statistical. When you throw a ball in the air, will
it come down? Yes, every time. That's physics. If you smoke four packs a
day, will you get lung cancer? The answer is maybe. We know that your
odds of getting lung cancer are much higher than if you didn't smoke, and
we can tell you what those odds (statistics) are, but we can't know with
certainty whether you as an individual will get lung cancer.

In nutrition research, untangling the relationship between diet and
health is not so straightforward. Humans live all sorts of different ways,
have different genetic backgrounds and eat all sorts of different foods.
Experimental limitations such as cost restraints, time constraints and
measurement error are significant obstacles. Perhaps most importantly
food, lifestyle and health interact through such complex, multifaceted
systems that establishing proof for any one factor and any one disease is
nearly impossible, even if you had the perfect set of subjects, unlimited
time and unlimited financial resources.

Because of these difficulties, we do research using many different
strategies. In some cases, we assess whether a hypothetical cause pro-
duces a hypothetical effect by observing and measuring the differences
that already exist between different groups of people. We might observe
and compare societies who consume different amounts of fat, then ob-
serve whether these differences correspond to similar differences in the
rates of breast cancer or osteoporosis or some other disease condition.
We might observe and compare the dietary characteristics of people who
already have the disease with a comparable group of people who don't
have the disease. We might observe and compare disease rates in 1950

A HOUSE OF PROTEINS

with disease rates in 1990, then observe whether any changes in disease
rates correspond to dietary changes.

In addition to observing what already exists, we might do an experi-
ment and intentionally intervene with a hypothetical treatment to see
what happens. We intervene, for example, when testing for the safety
and efficacy of drugs. One group of people is given the drug and a sec-
ond group a placebo (an inactive look-alike substance to please the
patient). Intervening with diet, however, is far more difficult, especially
if people aren't confined to a clinical setting, because then we must rely
on everyone to faithfully use the specified diets.

As we do observational and interventional research, we begin to amass
the findings and weigh the evidence for or against a certain hypothesis.
When the weight of the evidence favors an idea so strongly that it can no
longer be plausibly denied, we advance the idea as a likely truth. It is in
this way that I am advancing an argument for a whole foods, plant-based
diet. As you continue reading, realize that those seeking absolute proof
of optimal nutrition in one or two studies will be disappointed and con-
fused. However, I am confident that those seeking the truth regarding diet
and health by surveying the weight of the evidence from the variety of
available studies will be amazed and enlightened. There are several ideas
to keep in mind when determining the weight of the evidence, including
the following ideas.

CORRELATION VERSUS CAUSATION

In many studies, you will find that the words correlation and association
are used to describe a relationship between two factors, perhaps even in-
dicating a cause-and-effect relationship. This idea is featured prominently
in the China Study. We observed whether there were patterns of associa-
tions for different dietary, lifestyle and disease characteristics within the
survey of 65 counties, 130 villages and 6,500 adults and their families.
If protein consumption, for example, is higher among populations that
have a high incidence of liver cancer, we can say that protein is positively
correlated or associated with liver cancer incidence; as one goes up, the
other goes up. If protein intake is higher among populations that have a
low incidence of liver cancer, we can say that protein is inversely associ-
ated with liver cancer incidence. In other words, the two factors go in the
opposite direction; as one goes up, the other goes down.

In our hypothetical example, if protein is correlated with liver can-
cer incidence, this does not prove that protein causes or prevents liver

THE CHINA STUDY

cancer. A classic illustration of this difficulty is that countries with more
telephone poles often have a higher incidence of heart disease, and
many other diseases. Therefore, telephone poles and heart disease are
positively correlated. But this does not prove that telephone poles cause
heart disease. In effect, correlation does not equal causation.

This does not mean that correlations are useless. When they are
properly interpreted, correlations can be effectively used to study nu-
trition and health relationships. The China Study, for example, has
over 8,000 statistically significant correlations, and this is of immense
value. When so many correlations like this are available, researchers
can begin to identify patterns of relationships between diet, lifestyle
and disease. These patterns, in turn, are representative of how diet and
health processes, which are unusually complex, truly operate. However,
if someone wants proof that a single factor causes a single outcome, a
correlation is not good enough.

STATISTICAL SIGNIFICANCE

You might think that deciding whether or not two factors are correlated
is obvious — either they are or they aren't. But that isn't the case. When
you are looking at a large quantity of data, you have to undertake a sta-
tistical analysis to determine if two factors are correlated. The answer
isn't yes or no. It's a probability which we call statistical significance. Sta-
tistical significance is a measure of whether an observed experimental
effect is truly reliable or whether it is merely due to the play of chance.
If you flip a coin three times and it lands on heads each time, it's prob-
ably chance. If you flip it a hundred times and it lands on heads each
time, you can be pretty sure the coin has heads on both sides. That's the
concept behind statistical significance — it's the odds that the correlation
(or other finding) is real, that it isn't just random chance.

A finding is said to be statistically significant when there is less than
5% probability that it is due to chance. This means, for example, that
there is a 95% chance that we will get the same result if the study is
repeated. This 95% cutoff point is arbitrary, but it is the standard, none-
theless. Another arbitrary cutoff point is 99%. In this case, when the
result meets this test, it is said to be highly statistically significant. In the
discussions of diet and disease research in this book, statistical signifi-
cance pops up from time to time, and it can be used to help judge the
reliability, or "weight," of the evidence.

A HOUSE OF PROTEINS

MECHANISMS OF ACTION

Oftentimes correlations are considered more reliable if other research
shows that two correlated factors are biologically related. For example,
telephone poles and heart disease are positively correlated, but there is
no research that shows how telephone poles are biologically related to
heart disease. However, there is research that shows the processes by
which protein intake and liver cancer might be biologically and caus-
ally related (as you will see in chapter three). Knowing the process by
which something works in the body means knowing its "mechanism
of action." And knowing its mechanism of action strengthens the evi-
dence. Another way of saying this is that the two correlated factors are
related in a "biologically plausible" way. If a relationship is biologically
plausible, it is considered much more reliable.

METANALYSIS

Finally, we should understand the concept of a metanalysis. A met-
analysis tabulates the combined data from multiple studies and ana-
lyzes them as one data set. By accumulating and analyzing a large body
of combined data, the result can have considerably more weight. Met-
analysis findings are therefore more substantial than the findings of
single research studies, although, as with everything else, there may be
exceptions.

After obtaining the results from a variety of studies, we can then be-
gin to use these tools and concepts to assess the weight of the evidence.
Through this effort, we can begin to understand what is most likely to
be true, and we can behave accordingly. Alternative hypotheses no lon-
ger seem plausible, and we can be very confident in the result. Absolute
proof, in the technical sense, is unattainable and unimportant. But com-
mon sense proof (99% certainty) is attainable and critical. For example,
it was through this process of interpreting research that we formed our
beliefs regarding smoking and health. Smoking has never been "100%"
proven to cause lung cancer, but the odds that smoking is unrelated to
lung cancer are so astronomically low that the matter has long been
considered settled.

Turning Off Cancer

Americans dread cancer more than any other disease. Slowly and pain-
fully being consumed by cancer for months, even years, before passing
away is a terrifying prospect. This is why cancer is perhaps the most
feared of the major diseases.

So when the media reports a newly found chemical carcinogen, the
public takes notice and reacts quickly. Some carcinogens cause outright
panic. Such was the case a few years ago with Alar, a chemical that was
routinely sprayed on apples as a growth regulator. Shortly after a report
from the Natural Resources Defense Council (NRDC) titled "Intoler-
able Risk: Pesticides in Our Children's Food," 1 the television program
60 Minutes aired a segment on Alar. In February 1989 a representative
of NRDC said on CBS's 60 Minutes that the apple industry chemical was
"the most potent carcinogen in the food supply" 2 3

The public reaction was swift. One woman called state police to
chase down a school bus to confiscate her child's apple. 4 School systems
across the country, in New York, Los Angeles, Atlanta and Chicago,
among others, stopped serving apples and apple products. According to
John Rice, former chairman of the U.S. Apple Association, the apple in-
dustry took an economic walloping, losing over $250 million. 5 Finally,
in response to the public outcry, the production and use of Alar came to
a halt in June of 1989. 3

The Alar story is not uncommon. Over the past several decades, sev-
eral chemicals have been identified in the popular press as cancer-caus-
ing agents. You may have heard of some:

THE CHINA STUDY

• Aminotriazole (herbicide used on cranberry crops, causing the
"cranberry scare'" of 1959)

• DDT (widely known after Rachel Carson's book, Silent Spring)

• Nitrites (a meat preservative and color and flavor enhancer used in
hot dogs and bacon)

• Red Dye Number 2

• Artificial sweeteners (including cyclamates and saccharin)

• Dioxin (a contaminant of industrial processes and of Agent Or-
ange, a defoliant used during the Vietnam War)

• Anatoxin (a fungal toxin found on moldy peanuts and corn)

I know these unsavory chemicals quite well. I was a member of the
National Academy of Sciences Expert Panel on Saccharin and Food
Safety Policy (1978-79), which was charged with evaluating the poten-
tial danger of saccharin at a time when the public was up in arms after
the FDA proposed banning the artificial sweetener. I was one of the first
scientists to isolate dioxin; I have firsthand knowledge of the MIT lab
that did the key work on nitrites, and I spent many years researching
and publishing on anatoxin, one of the most carcinogenic chemicals
ever discovered — at least for rats.

But while these chemicals are significantly different in their proper-
ties, they all have a similar story with regard to cancer. In each and ev-
ery case, research has demonstrated that these chemicals may increase
cancer rates in experimental animals. The case of nitrites serves as an
excellent example.

THE HOT DOG MISSILE

If you hazard to call yourself "middle-aged" or older, when I say, "Ni-
trites, hot dogs and cancer," you might rock back in your chair, nod
your head, and say, "Oh yeah, I remember something about that." For
the younger folks — well, listen up, because history has a funny way of
repeating itself.

The time: the early 1970s. The scene: the Vietnam War was begin-
ning to wind down, Richard Nixon was about to be forever linked to
Watergate, the energy crisis was about to create lines at gas stations and
nitrite was becoming a headline word.

Sodium Nitrite: A meat preservative used since the 1920s. 6 It kills
bacteria and adds a happy pink color and desirable taste to hot
dogs, bacon and canned meat.

TURNING OFF CANCER

In 1970, the journal Nature reported that the nitrite we consume may
be reacting in our bodies to form nitrosamines. 7

Nitrosamines: A scary family of chemicals. No fewer than seven-
teen nitrosamines are "reasonably anticipated to be human car-
cinogens" by the U.S. National Toxicology Program. 8

Hold on a second. Why are these scary nitrosamines "anticipated to
be human carcinogens"? The short answer: animal experiments have
shown that as chemical exposure increases, incidence of cancer also
increases. But that's not adequate. We need a more complete answer.

Let's look at one nitrosamine, NSAR (N-nitrososarcosine). In one
study, twenty rats were divided into two groups, each exposed to a differ-
ent level of NSAR. The high-dose rats were given twice the amount that
the low-dose rats received. Of rats given the lower level of NSAR, just
over 35% of them died from throat cancer. Of rats given the higher levels,
100% died of cancer during the second year of the experiment. 9 " 11

How much NSAR did the rats get? Both groups of rats were given
an incredible amount. Let me translate the "low" dose by giving you a
little scenario. Let's say you go over to your friend's house to eat every
meal. This friend is sick of you and wants to give you throat cancer
by exposing you to NSAR. So he gives you the equivalent of the "low"
level given to the rats. You go to his house, and your friend offers you a
bologna sandwich that has a whole pound of bologna on it! You eat it.

He offers you another, and another, and another You'll have to eat

270,000 bologna sandwiches before your friend lets you leave. 9, 12 You
better like bologna, because your friend is going to have to feed you this
way every day for over thirty years! If he does this, you will have had
about as much exposure to NSAR (per body weight) as the rats in the
"low"-dose group.

Because higher cancer rates were also seen in mice as well as rats, us-
ing a variety of methods of exposure, NSAR is "reasonably anticipated"
to be a human carcinogen. Although no human studies were used to
make this evaluation, it is likely that a chemical such as this, which
consistently causes cancer in both mice and rats, can cause cancer in
humans at some level. It is impossible to know, however, what this
level of exposure might be, especially because the animal dosages are
so astronomical. Nonetheless, animal experiments alone are considered
enough to conclude that NSAR is "reasonably anticipated" to be a hu-
man carcinogen. 9

THE CHINA STUDY

So, in 1970, when an article in the prestigious journal Nature con-
cluded that nitrites help to form nitrosamines in the body, thereby im-
plying that they help to cause cancer, people became alarmed. Here was
the official line: "Reduction of human exposure to nitrites and certain
secondary amines, particularly in foods, may result in a decrease in
the incidence of human cancer." 7 Suddenly nitrites became a potential
killer. Because we humans get exposed to nitrites through consump-
tion of processed meat such as hot dogs and bacon, some products
came under fire. Hot dogs were an easy target. Besides containing addi-
tives like nitrites, hot dogs can be made out of ground-up lips, snouts,
spleens, tongues, throats and other "variety meats." 13 So as the nitrite/
nitrosamine issue heated up, hot dogs weren't looking so hot. Ralph
Nader had called hot dogs "among America's deadliest missiles." 14 Some
consumer advocacy groups were calling for a nitrite additive ban, and
government officials began a serious review of nitrite's potential health
problems. 3

The issue jolted forward again in 1978, when a study at the Massa-
chusetts Institute of Technology (MIT) found that nitrite increased lym-
phatic cancer in rats. The study as reported in a 1979 issue of Science, 15
found that, on average, rats fed nitrite got lymphatic cancer 10.2% of
the time, while animals not fed nitrite got cancer only 5.4% of the time.
This finding was enough to create a public uproar. Fierce debate ensued
in the government, industry and research communities. When the dust
settled, expert panels made recommendations, industry cut back on ni-
trite usage and the issue fell out of the spotlight.

To summarize the story: marginal scientific results can make very big
waves in the public when it comes to cancer-causing chemicals. A rise
in cancer incidence from 5% to 10% in rats fed large quantities of nitrite
caused an explosive controversy. Undoubtedly millions of dollars were
spent following the MIT study to investigate and discuss the findings.
And NSAR, a nitrosamine possibly formed from nitrite, was "reasonably
anticipated to be a human carcinogen" after several animal experiments
where exceptionally high levels of chemical were fed to animals for al-
most half their lifespan.

BACK TO PROTEIN

The point isn't that nitrite is safe. It is the mere possibility, however un-
likely it may be, that it could cause cancer that alarms the public. But
what if researchers produced considerably more impressive scientific

TURNING OFF CANCER

results that were far more substantial? What if there was a chemical that
experimentally turned on cancer in 100% of the test animals and its rela-
tive absence limited cancer to 0% of the animals? Furthermore, what if
this chemical were capable of acting in this way at routine levels of intake
and not the extraordinary levels used in the NSAR experiments? Finding
such a chemical would be the holy grail of cancer research. The implica-
tions for human health would be enormous. One would assume that this
chemical would be of considerably more concern than nitrite and Alar,
and even more significant than aflatoxin, a highly ranked carcinogen.

This is exactly what I saw in the Indian research paper 16 when I was
in the Philippines. The chemical was protein, fed to rats at levels that
are well within the range of normal consumption. Protein! These results
were more than startling. In the Indian study, when all the rats had been
predisposed to get liver cancer after being given aflatoxin, only the ani-
mals fed 20% protein got the cancer while those fed 5% got none.

Scientists, myself included, tend to be a skeptical bunch, especially
when confronted with eye-popping results. In fact, it is our responsibil-
ity as researchers to question and explore such provocative findings. We
might suspect that this finding was unique to rats exposed to aflatoxin
and for no other species, including humans. Maybe there were other
unknown nutrients that were affecting the data. Maybe my friend, the
distinguished MIT professor, was right; maybe the animal identities in
the Indian study got mixed up.

The questions begged for answers. To further study this question,
I sought and received the two National Institutes of Health (NIH)
research grants that I mentioned earlier. One was for a human study
the other for an experimental animal study. I did not "cry wolf in
either application by suggesting that protein might promote cancer.
I had everything to lose and nothing to gain by acting like a heretic.
Besides, I wasn't convinced that protein actually might be harmful. In
the experimental animal study, I proposed to investigate the "effect of
various factors [my italics] on aflatoxin metabolism." The human study
mostly focused on anatoxin's effects on liver cancer in the Philippines,
was briefly reviewed in the last chapter and was concluded after three
years. It was later renewed in a much more sophisticated study in China
(chapter four).

A study of this protein effect on tumor development had to be done ex-
tremely well. Anything less would not have convinced anyone, especially
my peers who would review my future request for renewed funding! In

THE CHINA STUDY

hindsight, we must have succeeded. The NIH funding for this study con-
tinued for the next nineteen years and led to additional funding from
other research agencies (American Cancer Society, the American Institute
for Cancer Research and the Cancer Research Foundation of America).
On these experimental animal findings alone, this project gave rise to
more than 100 scientific papers published in some of the best journals,
many public presentations and several invitations to participate on expert
panels.

ANIMAL RIGHTS

The rest of this chapter concerns experimental animal research, all
of which included rodents (rats and mice). I know well that many
oppose the use of experimental animals in research. I respect this
concern. I respectfully suggest, however, that you consider this:
very likely, I would not be advocating a plant-based diet today if
it were not for these animal experiments. The findings and the
principles derived from these animal studies greatly contributed
to my interpretations of my later work, including the China Study,
as you will come to see.

One obvious question regarding this issue is whether there
was an alternative way to get the same information without us-
ing experimental animals. To date, I have found none, even after
seeking advice from my "animal rights" colleagues. These experi-
mental animal studies elaborated some very important principles
of cancer causation not obtainable in human-based studies. These
principles now have enormous potential to benefit all of our fel-
low creatures, our environment and ourselves.

THREE STAGES OF CANCER

Cancer proceeds through three stages: initiation, promotion and progres-
sion. To use a rough analogy, the cancer process is similar to planting a
lawn. Initiation is when you put the seeds in the soil, promotion is when
the grass starts to grow and progression is when the grass gets completely
out of control, invading the driveway, the shrubbery and the sidewalk.

So what is the process that successfully "implants" the grass seed in
the soil in the first place, i.e., initiates cancer-prone cells? Chemicals
that do this are called carcinogens. These chemicals are most often

TURNING OFF CANCER 49
CHART 3.1: TUMOR INITIATION BY AFLATOXIN INSIDE A LIVER CELL

(6) A cell multiplies
before the damaged
DNA is repaired and
permanently damaged,
cancerous cells arise

Cancerous
' — \Cells

Cancer Initiation

After entering our cells (Step 1), most carcinogens do not, themselves, initiate the cancer
process. They first must be converted to products that are more reactive (Steps 2 & 3), with
the help of critically important enzymes. These carcinogen products then bind tightly to
the cell's DNA to form carcinogen-DNA complexes, or adducts (Step 4).

Unless repaired or removed, carcinogen-DNA adducts have the potential to create chaos
with the genetic workings of the cell. But nature is smart. These adducts can be repaired,
and most adducts are repaired fairly quickly (Step 5). However, if they remain in place
while cells are dividing to form new "daughter" cells, genetic damage occurs and this new
genetic defect (or mutation) is passed on to all new cells formed thereafter (Step 6). "

the byproducts of industrial processes, although small amounts may
be formed in nature, as is the case with aflatoxin. These carcinogens
genetically transform, or mutate, normal cells into cancer-prone cells.
A mutation involves permanent alteration of the genes of the cell, with
damage to its DNA.

The entire initiation stage (Chart 3.1) can take place in a very short
period of time, even minutes. It is the time required for the chemical
carcinogen to be consumed, absorbed into the blood, transported into
cells, changed into its active product, bonded to DNA and passed on to
the daughter cells. When the new daughter cells are formed, the process
is complete. These daughter cells and all their progeny will forever be
genetically damaged, giving rise to the potential for cancer. Except in rare
instances, completion of the initiation phase is considered irreversible.

THE CHINA STUDY

At this point in our lawn analogy, the grass seeds have been put in
the soil and are ready to germinate. Initiation is complete. The second
growth stage is called promotion. Like seeds ready to sprout blades of
grass and turn into a green lawn, our newly formed cancer-prone cells
are ready to grow and multiply until they become a visibly detectable
cancer. This stage occurs over a far longer period of time than initiation,
often many years for humans. It is when the newly initiated cluster mul-
tiplies and grows into larger and larger masses and a clinically visible
tumor is formed.

But just like seeds in the soil, the initial cancer cells will not grow and
multiply unless the right conditions are met. The seeds in the soil, for
example, need a healthy amount of water, sunlight and other nutrients
before they make a full lawn. If any of these factors are denied or are
missing, the seeds will not grow. If any of these factors are missing after
growth starts, the new seedlings will become dormant, while awaiting
further supply of the missing factors. This is one of the most profound
features of promotion. Promotion is reversible, depending on whether the
early cancer growth is given the right conditions in which to grow. This is
where certain dietary factors become so important. These dietary fac-
tors, called promoters, feed cancer growth. Other dietary factors, called
anti-promoters, slow cancer growth. Cancer growth flourishes when
there are more promoters than anti-promoters; when anti-promoters
prevail cancer growth slows or stops. It is a push-pull process. The pro-
found importance of this reversibility cannot be overemphasized.

The third phase, progression, begins when a bunch of advanced cancer
cells progress in their growth until they have done their final damage. It
is like the fully-grown lawn invading everything around it: the garden,
driveway and sidewalk. Similarly, a developing cancer tumor may wander
away from its initial site in the body and invade neighboring or distant
tissues. When the cancer takes on these deadly properties, it is considered
malignant. When it actually breaks away from its initial home and wan-
ders, it is metastasizing. This final stage of cancer results in death.

At the start of our research, the stages of cancer formation were
known only in vague outline. But we knew enough about these stages
of cancer to be able to structure our research more intelligently. We had
no shortage of questions. Could we confirm the findings from India that
a low-protein diet represses tumor formation? More importantly, why
does protein affect the cancer process? What are the mechanisms; that
is, how does protein work? With plenty of questions to be answered, we

TURNING OFF CANCER

went about our experimental studies meticulously and in depth in order
to obtain results that would withstand the harshest of scrutiny.

PROTEIN AND INITIATION

How does protein intake affect cancer initiation? Our first test was to
see whether protein intake affected the enzyme principally responsible
for aflatoxin metabolism, the mixed function oxidase (MFO). This en-
zyme is very complex because it also metabolizes pharmaceuticals and
other chemicals, friend or foe to the body. Paradoxically this enzyme
both detoxifies and activates aflatoxin. It is an extraordinary transfor-
mation substance.

THE ENZYME "FACTORY"

In a simplistic way, the MFO enzyme system can be thought of as a factory
within the industrious workings of the cell. Various chemical "raw materi-
als" are fed into the factory, where all the complex reactions are performed.
The raw materials may be disassembled or assembled. After a transforming
process, the "raw material" chemicals are ready to be shipped out of the
factory as mostly normal, safe products. But there also may be byproducts
of these complex processes that are exceptionally dangerous. Think of the
smokestack at a real-life factory. If someone told you to stick your face down
a smokestack and breathe deeply for a couple hours, you'd refuse. Within
the cell, the dangerous byproducts, if not held in check, are the highly reac-
tive aflatoxin metabolites that go on to attack the cell's DNA and damage its
genetic blueprint.

THE CHINA STUDY

At the time we started our research, we hypothesized that the protein
we consume alters tumor growth by changing how anatoxin is detoxi-
fied by the enzymes present in the liver.

We initially determined whether the amount of protein that we eat
could change this enzyme activity. After a series of experiments (Chart
3.2 18 ), the answer was clear. Enzyme activity could be easily modified
simply by changing the level of protein intake. 18-21

Decreasing protein intake like that done in the original research in
India (20% to 5%) not only greatly decreased enzyme activity, but did
so very quickly. 22 What does this mean? Decreasing enzyme activity via
low-protein diets implied that less anatoxin was being transformed into
the dangerous anatoxin metabolite that had the potential to bind and to
mutate the DNA.

We decided to test this implication: did a low-protein diet actually
decrease the binding of anatoxin product to DNA, resulting in fewer
adducts? An undergraduate student in my lab, Rachel Preston, did the
experiment (Chart 3.3) and showed that the lower the protein intake,
the lower the amount of aflatoxin-DNA adducts. 23

We now had impressive evidence that low protein intake could mark-
edly decrease enzyme activity and prevent dangerous carcinogen bind-
ing to DNA. These were very impressive findings, to be sure. It might
even be enough information to "explain" how consuming less protein
leads to less cancer. But we wanted to know more and be doubly assured
of this effect, so we continued to look for other explanations. As time
passed, we were to learn something really quite remarkable. Almost ev-

CHART 3.2: EFFECT OF DIETARY PROTEIN ON ENZYME ACTIVITY

250 -A

76% decrease

20% Protein

5% Protein

TURNING OFF CANCER

CHART 3.3: DECREASE IN CARCINOGEN BINDING TO NUCLEUS
COMPONENTS CAUSED BY LOW-PROTEIN FEEDING

DNA Chromatin 'rotein

ery time we searched for a way, or mechanism, by which protein works
to produce its effects, we found one! For example, we came to discover
that low-protein diets, or their equivalents, reduce tumors by the fol-
lowing mechanisms:

• less aflatoxin entered the cell 21 " 26

• cells multiplied more slowly 18

• multiple changes occurred within the enzyme complex to reduce
its activity 27

• the quantity of critical components of the relevant enzymes was
reduced 2829

• less aflatoxin-DNA adducts were formed 23 ' 30

The fact that we found more than one way (mechanism) that low-
protein diets work was eye-opening. It added a great deal of weight to
the results of the Indian researchers. It also suggested that biological
effects, although often described as operating through single reactions,
more likely operate through a large number of varied simultaneous re-
actions, very likely acting in a highly integrated and concerted manner.
Could this mean that the body had lots of backup systems in case one
was bypassed in some way? As research unfolded in the subsequent
years, the truth of this thesis became increasingly evident.

From our extensive research, one idea seemed to be clear: lower pro-
tein intake dramatically decreased tumor initiation. This finding, even
though well substantiated, would be enormously provocative for many
people.

THE CHINA STUDY

PROTEIN AND PROMOTION

To go back to the lawn analogy, sowing the grass seeds in the soil was the
initiation process. We found, conclusively, through a number of experi-
ments, that a low-protein diet could decrease, at the time of planting,
the number of seeds in our "cancerous" lawn. That was an incredible
finding, but we needed to do more. We wondered: what happens during
the promotion stage of cancer, the all-important reversible stage? Would
the benefits of low protein intake achieved during initiation continue
through promotion?

Practically speaking, it was difficult to study this stage of cancer be-
cause of time and money. It is an expensive study that allows rats to live
until they develop full tumors. Each such experiment would take more
than two years (the normal lifetime of rats) and would have cost well
over $100,000 (even more money today). To answer the many ques-
tions that we had, we could not proceed by studying full tumor develop-
ment; I would still be in the lab, thirty-five years later!

This is when we learned of some exciting work just published by oth-
ers 31 that showed how to measure tiny clusters of cancer-like cells that
appear right after initiation is complete. These little microscopic cell
clusters were called foci.

Foci are precursor clusters of cells that grow into tumors. Although
most foci do not become full-blown tumor cells, they are predictive of
tumor development.

By watching foci develop and measuring how many there are and how
big they become, 32 we could learn indirectly how tumors also develop
and what effect protein might have. By studying the effects of protein
on the promotion of foci instead of tumors we could avoid spending a
lifetime and a few million dollars working in the lab.

What we found was truly remarkable. Foci development was almost
entirely dependent on how much protein was consumed, regardless oj how
much aflatoxin was consumed!

This was documented in many interesting ways, first done by my
graduate students Scott Appleton 33 and George DunaiP 4 (a typical com-
parison is shown in Chart 3.4). After initiation with aflatoxin, foci grew
(were promoted) far more with the 20% protein diet than with the 5%
protein diet. 33,34

Up to this point, all of the animals were exposed to the same amount of
aflatoxin. But what if the initial aflatoxin exposure is varied? Would protein

TURNING OFF CANCER

CHART 3.4: DIETARY PROTEIN AND FOCI FORMATION

5% 20%

Dietary Protein Level

CHART 3.5: CARCINOGEN DOSE VERSUS PROTEIN INTAKE

HighAF Low AF

Low Protein High Protein

THE CHINA STUDY

still have an effect? We investigated this question by giving two groups
of rats either a high-aflatoxin dose or a low-aflatoxin dose, along with a
standard baseline diet. Because of this the two groups of rats were starting
the cancer process with different amounts of initiated, cancerous "seeds."
Then, during the promotion phase, we fed a low-protein diet to the high-
aflatoxin dose groups and a high-protein diet to the low-aflatoxin dose
group. We wondered whether the animals that start with lots of cancerous
seeds are able to overcome their predicament by eating a low-protein diet.

Again, the results were remarkable (Chart 3.5). Animals starting with
the most cancer initiation (high-aflatoxin dose) developed substantially
less foci when fed the 5% protein diet. In contrast, animals initiated with
a low-aflatoxin dose actually produced substantially more foci when sub-
sequently fed the 20% protein diet.

A principle was being established. Foci development, initially deter-
mined by the amount of the carcinogen exposure, is actually controlled
far more by dietary protein consumed during promotion. Protein dur-
ing promotion trumps the carcinogen, regardless of initial exposure.

With this background information we designed a much more sub-
stantial experiment. Here is a step-by-step sequence of experiments,
carried out by my graduate student Linda Youngman. 35 All animals were
dosed with the same amount of carcinogen, then alternately fed either
5% or 20% dietary protein during the twelve-week promotion stage.
We divided this twelve -week promotion stage into four periods of three
weeks each. Period 1 represents weeks one to three, period 2 represents
weeks four to six, and so on.

When animals were fed the 20% protein diet during periods 1 and 2
(20-20), foci continued to enlarge, as expected. But when animals were
switched to the low-protein diet at the beginning of period 3 (20-20-
5), there was a sharp decrease in foci development. And, when animals
were subsequently switched back to the 20% protein diet during period
4 (20-20-5-20), foci development was turned on once again.

In another experiment, in animals fed 20% dietary protein during
period 1 but switched to 5% dietary protein during period 2 (20-5), foci
development was sharply decreased. But when these animals were re-
turned to 20% dietary protein during period 3 (20-5-20), we again saw
the dramatic power of dietary protein to promote foci development.

These several experiments, taken together, were quite profound. Foci
growth could be reversed, up and down, by switching the amount of
protein being consumed, and at all stages of foci development.

TURNING OFF CANCER

These experiments also demonstrated that the body could "remem-
ber" early carcinogen insults, 35, 16 even though they might then lie
dormant with low protein intake. That is, exposure to anatoxin left a
genetic "imprint" that remained dormant with 5% dietary protein until
nine weeks later when this imprint reawakened to form foci with 20%
dietary protein. In simple terms, the body holds a grudge. It suggests
that if we are exposed in the past to a carcinogen that initiates a bit of
cancer that remains dormant, this cancer can still be "reawakened" by
bad nutrition some time later.

These studies showed that cancer development is modified by relative-
ly modest changes in protein consumption. But how much protein is too
much or too little? Using rats, we investigated a range of 4-24% dietary
protein (Chart 3.6 37 )- Foci did not develop with up to about 10% dietary
protein. Beyond 10%, foci development increased dramatically with in-
creases in dietary protein. The results were later repeated a second time in
my laboratory by a visiting professor from Japan, Fumiyiki Horio. 38

CHART 3.6: FOCI PROMOTION BY DIETARY PROTEIN

80
70

~ 60
c

o. 50
_o

I 40
o

20
10

4 6 8 10 12 14 20
% Dietary Protein

THE CHINA STUDY

The most significant finding of this experiment was this: foci devel-
oped only when the animals met or exceeded the amount of dietary
protein (12%) needed to satisfy their body growth rate. 39 That is, when
the animals met and surpassed their requirement for protein, disease
onset began.

This finding may have considerable relevance for humans even
though these were rat studies. I say this because the protein required
for growth in young rats and humans as well as the protein required to
maintain health for adult rats and humans is remarkably similar. 40 41

According to the recommended daily allowance (RDA) for protein
consumption, we humans should be getting about 10% of our energy
from protein. This is considerably more than the actual amount required.
But because requirements may vary from individual to individual, 10%
dietary protein is recommended to insure adequate intake for virtually
all people. What do most of us routinely consume? Remarkably it is
considerably more than the recommended 10%. The average American
consumes 15-16% protein. Does this place us at risk for getting cancer?
These animal studies hint that it does.

Ten percent dietary protein is equivalent to eating about 50-60 grams
of protein per day, depending on body weight and total calorie intake. The
national average of 15-16% is about 70-100 grams of protein per day, with
men at the upper part of the range and women at the lower end. In food
terms, there are about twelve grams of protein in 100 calories of spinach
(fifteen ounces) and five grams of protein in 100 calories of raw chick peas
(just over two tablespoons). There are about thirteen grams of protein in
100 calories of porterhouse steak (just over one and a half ounces).

Yet another question was whether protein intake could modify the
all-important relationship between anatoxin dose and foci formation.
A chemical is usually not considered a carcinogen unless higher doses
yield higher incidences of cancer. For example, as the anatoxin dose
becomes greater, foci and tumor growth should be correspondingly
greater. If an increasing response is not observed for a suspect chemical
carcinogen, serious doubt arises whether it really is carcinogenic.

To investigate this dose-response question, ten groups of rats were
administered increasing doses of anatoxin, then fed either regular levels
(20%) or low levels (5-10%) of protein during the promotion period
(Chart 3.7 34 ).

In the animals fed the 20% level of protein, foci increased in number and
size, as expected, as the anatoxin dose was increased. The dose-response

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CHART 3.7: AFLATOXIN DOSE— FOCI RESPONSE

-m- 20% Protein
5% Protein

200 235 275 300 350
Aflatoxin Dose (mcg/kg body weight/day)

relationship was strong and clear. However, in the animals fed 5% protein,
the dose-response curve completely disappeared. There was no foci response,
even when animals were given the maximum tolerated aflatoxin dose. This
was yet another result demonstrating that a low-protein diet could over-
ride the cancer-causing effect of a very powerful carcinogen, aflatoxin.

Is it possible that chemical carcinogens, in general, do not cause
cancer unless the nutritional conditions are "right"? Is it possible that,
for much of our lives, we are being exposed to small amounts of cancer-
causing chemicals, but cancer does not occur unless we consume foods
that promote and nurture tumor development? Can we control cancer
through nutrition?

NOT ALL PROTEINS ARE ALIKE

If you have followed the story so far, you have seen how provocative
these findings are. Controlling cancer through nutrition was, and still
is, a radical idea. But as if this weren't enough, one more issue would
yield explosive information: did it make any difference what type of
protein was used in these experiments? For all of these experiments,
we were using casein, which makes up 87% of cow's milk protein. So
the next logical question was whether plant protein, tested in the same
way, has the same effect on cancer promotion as casein. The answer is
an astonishing "NO." In these experiments, plant protein did not promote
cancer growth, even at the higher levels of intake. An undergraduate pre-
medical student doing an honors degree with me, David Schulsinger,
did the study (Chart Itf 2 ). Gluten, the protein of wheat, did not produce
the same result as casein, even when Jed at the same 20% level.

THE CHINA STUDY
CHART 3.8: PROTEIN TYPE AND FOCI RESPONSE

■ 20% Casein

■ 20% Gluten

□ 5% Casein

Protein Type

We also examined whether soy protein had the same effect as casein
on foci development. Rats fed 20% soy protein diets did not form early foci,
just like the 20% wheat protein diets. Suddenly protein, milk protein in this
case, wasn't looking so good. We had discovered that low protein intake
reduces cancer initiation and works in multiple synchronous ways. As if
that weren't enough, we were finding that high protein intake, in excess
of the amount needed for growth, promotes cancer after initiation. Like
flipping a light switch on and off, we could control cancer promotion
merely by changing levels of protein, regardless of initial carcinogen
exposure. But the cancer-promoting factor in this case was cow's milk
protein. It was difficult enough for my colleagues to accept the idea that
protein might help cancer grow, but cow's milk protein? Was I crazy?

ADDITIONAL QUESTIONS

For those readers who want to know somewhat more, I've includ-
ed a few questions in Appendix A.

THE GRAND FINALE

Thus far we had relied on experiments where we measured only the ear-
ly indicators of tumor development, the early cancer-like foci. Now, it
was time to do the big study, the one where we would measure complete
tumor formation. We organized a very large study of several hundred
rats and examined tumor formation over their lifetimes using several
different approaches. 36 43

TURNING OFF CANCER

The effects of protein feeding on tumor development were nothing
less than spectacular. Rats generally live for about two years, thus the
study was 100 weeks in length. All animals that were administered afla-
toxin and fed the regular 20% levels of casein either were dead or near
death from liver tumors at 100 weeks. 36 43 All animals administered the
same level of anatoxin but fed the low 5% protein diet were alive, active
and thrifty with sleek hair coats at 100 weeks. This was a virtual 100 to
0 score, something almost never seen in research and almost identical
to the original research in India. 16

In this same experiment, 36 we switched the diets of some rats at either
forty or sixty weeks, to again investigate the reversibility of cancer pro-
motion. Animals switched from a high-protein to a low-protein diet had
significantly less tumor growth (35%-40% less!) than animals fed a high-
protein diet. Animals switched from a low-protein diet to a high-protein

CHART 3.9A: TUMOR DEVELOPMENT AT 100 WEEKS

OJ
CC

o
E

3330

2350

240

14% 22%

CHART 3.9B: EARLY FOCI, "LIFETIME'

o - / f l i tl v (

% Dietary Casein

THE CHINA STUDY

diet halfway through their lifetime started growing tumors again. These
findings on full-blown tumors confirmed our earlier findings using foci.
Namely, nutritional manipulation can turn cancer "on" and "off."

We also measured early foci in these "lifetime" studies to see if their
response to dietary protein was similar to that for tumor response. The
correspondence between foci growth and tumor growth could not have
been greater (Chart 3.9a). 36,43

How much more did we need to find out? I would never have dreamed
that our results up to this point would be so incredibly consistent, bio-
logically plausible and statistically significant. We had fully confirmed the
original work from India and had done it in exceptional depth.

Let there be no doubt: cow's milk protein is an exceptionally potent
cancer promoter in rats dosed with aflatoxin. The fact that this promotion
effect occurs at dietary protein levels (10-20%) commonly used both in
rodents and humans makes it especially tantalizing — and provocative.

OTHER CANCERS, OTHER CARCINOGENS

Okay, so here's the central question: how does this research apply to hu-
man health and human liver cancer in particular? One way to investigate
this question is to research other species, other carcinogens and other
organs. If casein's effect on cancer is consistent across these categories,
it becomes more likely that humans better take note. So our research be-
came broader in scope, to see whether our discoveries would hold up.

While our rat studies were underway, studies were published 44 ' 45
claiming that chronic infection with hepatitis B virus (HBV) was the
major risk factor for human liver cancer. It was thought that people who
remained chronically infected with HBV had twenty to forty times the
risk of getting liver cancer.

Over the years, considerable research had been done on how this
virus causes liver cancer. 46 In effect, a piece of the virus gene inserts
itself into the genetic material of the mouse liver where it initiates liver
cancer. When this is done experimentally the animals are considered
transgenic.

Virtually all of the research done in other laboratories on HBV trans-
genic mice — and there was a lot of it — was done primarily to understand
the molecular mechanism by which HBV worked. No attention was
given to nutrition and its effect on tumor development. I watched with
some amusement for several years how one community of researchers
argued for aflatoxin as the key cause of human liver cancer and another

TURNING OFF CANCER

community argued for HBV No one in either community dared to sug-
gest that nutrition had anything to do with this disease.

We wanted to know about the effect of casein on HBV-induced liver
cancer in mice. This was a big step. It went beyond anatoxin as a carcino-
gen and rats as a species. A brilliant young graduate student from China in
my group, Jifan Hu, initiated studies to answer this question and was later
joined by Dr. Zhiqiang Cheng. We needed a colony of these transgenic
mice. There were two such "breeds" of mice, one living in Lajolla, Califor-
nia, the other in Rockville, Maryland. Each strain had a different piece of
HBV gene stuck in the genes of their livers, and each was therefore highly
prone to liver cancer. I contacted the responsible researchers and inquired
about their helping us to establish our own mouse colony. Both research
groups asked what we wanted to do and both were inclined to think that
studying the protein effect was foolish. I also sought a research grant to
study this question and it was rejected. The reviewers did not take kindly
to the idea of a nutritional effect on a virus-induced cancer, especially of
a dietary protein effect. I was beginning to wonder: was I now being too
explicit in questioning the mythical health value of protein? The reviews
of the grant proposal certainly indicated this possibility.

We eventually obtained funding, did the study on both strains of
mice and got essentially the same result as we did with the rats.* 7 * 8 You can
see the results for yourself. The adjoining picture (Chart 3.10 47 ) shows
what a cross-section of the mouse livers looks like under a microscope.
The dark-colored material is indicative of cancer development (ignore
the "hole"; that's only a cross-section of a vein). There is intense early
cancer formation in the 22% casein animals (D), much less in the 14%
casein animals (C), and none in the 6% casein animals (B); the remain-
ing picture (A) shows a liver having no virus gene (the control).

The adjoining graph (Chart 3. II 47 ) shows the expression (activity) of
two HBV genes that cause cancer inserted in the mouse liver. Both the
picture and the graph show the same thing: the 22% casein diet turned
on expression of the viral gene to cause cancer, whereas the 6% casein
diet showed almost no such activity.

By this time, we had more than enough information to conclude that
casein, that sacred protein of cow's milk, dramatically promotes liver
cancer in:

• rats dosed with anatoxin

• mice infected with HBV

THE CHINA STUDY

CHART 3.10: DIETARY PROTEIN EFFECT ON GENETICALLY-BASED
(HBV) LIVER CANCER (MICE)

Non-transgenic Mice
(Control) with 22%
Casein Diet

>»o 1 o *'.0.-

*{ - , s . '<> «...

Transgenic Mice with
14% Casein Diet

Transgenic Mice with
6% Casein Diet

. <

■ r

Transgenic Mice with
22% Casein Diet

CHART 3.1 1: DIETARY PROTEIN EFFECT ON GENE EXPRESSION (MICE)

■

□

HBV Gene A

HBV Gene B

TURNING OFF CANCER

Not only are these effects substantial, but we also discovered a net-
work of complementary ways by which they worked.

Next question: can we generalize these findings to other cancers and
to other carcinogens? At the University of Illinois Medical Center in
Chicago, another research group was working with mammary (breast)
cancer in rats. 49 " 51 This research showed that increasing intakes of ca-
sein promoted the development of mammary (breast) cancer. They
found that higher casein intake:

• promotes breast cancer in rats dosed with two experimental car-
cinogens (7,12-dimethybenz(a)anthracene (DBMA) and N-ni-
troso-methylurea (NMU))

• operates through a network of reactions that combine to increase
cancer

• operates through the same female hormone system that operates in
humans

LARGER IMPLICATIONS

An impressively consistent pattern was beginning to emerge. For two
different organs, four different carcinogens and two different species,
casein promotes cancer growth while using a highly integrated system
of mechanisms. It is a powerful, convincing and consistent effect. For
example, casein affects the way cells interact with carcinogens, the way
DNA reacts with carcinogens and the way cancerous cells grow. The
depth and consistency of these findings strongly suggest that they are
relevant for humans, for four reasons. First, rats and humans have an
almost identical need for protein. Second, protein operates in humans
virtually the same way it does in rats. Third, the level of protein intake
causing tumor growth is the same level that humans consume. And
fourth, in both rodents and humans the initiation stage is far less im-
portant than the promotion stage of cancer. This is because we are very
likely "dosed" with a certain amount of carcinogens in our everyday
lives, but whether they lead to full tumors depends on their promotion,
or lack thereof.

Even though I became convinced that increasing casein intake pro-
motes cancer, I still had to be wary of generalizing too much. This was an
exceptionally provocative finding that drew fierce skepticism. But these
findings nonetheless were a hint of things to come. I wanted to broaden
my evidence still more. What effect did other nutrients have on can-

THE CHINA STUDY

cer, and how did they interact with different carcinogens and different
organs? Might the effects of other nutrients, carcinogens or organs
cancel each other, or might there be consistency of effect for nutrients
within certain types of food? Would promotion continue to be revers-
ible? If so, cancer might be readily controlled, even reversed, simply by
decreasing the intakes of the promoting nutrients and/or increasing the
intakes of the anti-promoting nutrients.

We initiated more studies using several different nutrients, including
fish protein, dietary fats and the antioxidants known as carotenoids.
A couple of excellent graduate students of mine, Tom O'Connor and
Youping He, measured the ability of these nutrients to affect liver and
pancreatic cancer. The results of these, and many other studies, showed
nutrition to be far more important in controlling cancer promotion than the
dose of the initiating carcinogen. The idea that nutrients primarily affect
tumor development during promotion was beginning to appear to be a
general property of nutrition and cancer relationships. The Journal of
the National Cancer Institute, which is the official publication of the U.S.
National Cancer Institute, took note of these studies and featured some
of our findings on its cover. 52

Furthermore, a pattern was beginning to emerge: nutrients from ani-
mal-based foods increased tumor development while nutrients from plant-
based foods decreased tumor development. In our large lifetime study of
rats with aflatoxin-induced tumors, the pattern was consistent. In mice
with hepatitis B virus-altered genes, the pattern was consistent. In stud-
ies done by another research group, with breast cancer and different car-
cinogens, the pattern was consistent. In studies of pancreatic cancer and
other nutrients, the pattern was consistent. 52 53 In studies on carotenoid
antioxidants and cancer initiation, the pattern was consistent. 54 55 From
the first stage of cancer initiation to the second stage of cancer promo-
tion, the pattern was consistent. From one mechanism to another, the
pattern was consistent.

So much consistency was stunningly impressive, but one aspect of
this research demanded that we remain cautious: all this evidence was
gathered in experimental animal studies. Although there are strong argu-
ments that these provocative findings are qualitatively relevant to human
health, we cannot know the quantitative relevance. In other words, are
these principles regarding animal protein and cancer critically important
for all humans in all situations, or are they merely marginally important
for a minority of people in fairly unique situations? Are these prin-

TURNING OFF CANCER

ciples involved in one thousand human cancers every year, one million
human cancers every year, or more? We need direct evidence from hu-
man research. Ideally, this evidence would be gathered with rigorous
methodology and would investigate dietary patterns comprehensively
using large numbers of people who had similar lifestyles, similar genetic
backgrounds, and yet had widely varying incidences of disease.

Having the opportunity to do such a study is rare, at best, but by
incredibly good luck we were given exactly the opportunity we needed.
In 1980 I had the good fortune of welcoming in my laboratory a most
personable and professional scientist from mainland China, Dr. Junshi
Chen. With this remarkable man, opportunities arose to search for some
larger truths. We were given the chance to do a human study that would
take all of these principles we had begun to uncover in the lab to the
next level. It was time to study the role of nutrition, lifestyle and disease
in the most comprehensive manner ever undertaken in the history of
medicine. We were on to the China Study.

Lessons from China

A SNAPSHOT IN TIME

Have you ever had the sensation of wanting to permanently capture a
moment? Such moments can grip you in a way you will never forget.
For some people, those moments center on family, close friends or re-
lated activities; for others those moments may center on nature, spiri-
tuality or religion. For most of us, I suspect, it can be a little of each.
They become the personal moments, both happy and sad, which define
our memories. It's these moments in which everything just "comes
together." They are the snapshots of time that define much of our life
experience.

The value of a snapshot of time is not lost on researchers either. We
construct experiments, hoping to preserve and analyze the specific de-
tails of a certain moment for years to come. I was fortunate enough to be
privy to such an opportunity in the early 1980s, after a distinguished se-
nior scientist from China, Dr. Junshi Chen, came to Cornell to work in
my lab. He was deputy director of China's premier health research labo-
ratory and one of the first handful of Chinese scholars to visit the U.S.
following the establishment of relations between our two countries.

THE CANCER ATLAS

In the early 1970s, the premier of China, Chou EnLai, was dying of
cancer. In the grips of this terminal disease, Premier Chou initiated a
nationwide survey to collect information about a disease that was not

THE CHINA STUDY

well understood. It was to be a monumental survey of death rates for
twelve different kinds of cancer for more than 2,400 Chinese counties
and 880 million (96%) of their citizens. The survey was remarkable in
many ways. It involved 650,000 workers, the most ambitious biomedi-
cal research project ever undertaken. The end result of the survey was a
beautiful, color-coded atlas showing where certain types of cancer were
high and where they were almost nonexistent. 1

CHART 4.1 : SAMPLE CANCER ATLAS IN CHINA

This atlas made it clear that in China cancer was geographically lo-
calized. Some cancers were much more common in some places than
in others. Earlier studies had set the stage for this idea, showing that
cancer incidence also varies widely between different countries. 2-4 But
these China data were more remarkable because the geographic varia-
tions in cancer rates were much greater (Chart 4.2). They also occurred
in a country where 87% of the population is the same ethnic group, the
Han people.

LESSONS FROM CHINA 71

CHART 4.2. RANGE OF CANCER RATES IN CHINESE COUNTIES

Cancer Site

Males

Females

All Cancers

35-721

35-491

Nasopharynx

0-75

0-26

Esophagus

1-435

0-286

Stomach

6-386

2-141

Liver

7-248

3-67

Colorectal

2-67

2-61

Lung

3-59

0-26

Breast

0-20

*Age-adjusted death rates, representing # cases/100,000 people/year

Why was there such a massive variation in cancer rates among dif-
ferent counties when genetic backgrounds were similar from place to
place? Might it be possible that cancer is largely due to environmental/
lifestyle factors, and not genetics? A few prominent scientists had al-
ready reached that conclusion. The authors of a major review on diet
and cancer, prepared for the U.S. Congress in 1981, estimated that ge-
netics only determines about 2-3% oj the total cancer risk*

The data behind the China cancer atlas were profound. The coun-
ties with the highest rates of some cancers were more than 100 times
greater than counties with the lowest rates of these cancers. These
are truly remarkable figures. By way of comparison, we in the U.S.
see, at most, two to three times the cancer rates from one part of the
country to another.

In fact, very small and relatively unimportant differences in cancer
rates make big news, big money and big politics. There has been a long-
standing story in my state of New York about the increased rates of
breast cancer in Long Island. Large amounts of money (about $30 mil-
lion 5 ) and years and years of work have been spent examining the issue.
What sorts of rates were causing such a furor? Two counties in Long Is-
land had rates of breast cancer only 10-20% higher than the state aver-
age. This difference was enough to make front-page news, scare people
and move politicians to action. Contrast this with the findings in China
where some parts of the country had cancer rates 100 times (10,000%)
higher than others.

THE CHINA STUDY

Because China is relatively homogenous genetically, it was clear that
these differences had to be explained by environmental causes. This
raised a number of critical questions:

• Why was cancer so high in some rural Chinese counties and not in
others?

• Why were these differences so incredibly large?

• Why was overall cancer, in the aggregate, less common in China
than in the U.S.?

The more Dr. Chen and I talked, the more we wished that we had
a snapshot in time of the dietary and environmental conditions in ru-
ral China. If only we could look into these people's lives, note what
they eat, how they live, what is in their blood and their urine and how
they die. If only we could construct a picture of their experience with
unprecedented clarity and detail so that we could study it for years to
come. If we could do that, we might be able to offer some answers to
our "why" questions.

Occasionally science, politics and financing come together in a way
that allows a truly extraordinary study to take place. This happened for
us, and we got the opportunity to do everything we wanted, and more.
We were able to create the most comprehensive snapshot of diet, life-
style and disease ever taken.

PULLING IT TOGETHER

We assembled a world-class scientific team. There was Dr. Chen, who
was the deputy director of the most significant government diet and
health research laboratory in all of China. We enlisted Dr. Junyao Li,
one of the authors of the Cancer Atlas Survey and a key scientist in Chi-
na's Academy of Medical Sciences in the Ministry of Health. The third
member was Richard Peto of Oxford University Considered one of the
premier epidemiologists in the world, Peto has since been knighted and
has received several awards for cancer research. I rounded out the team
as the Project Director.

Everything was coming together. It was to be the first major research
project between China and the United States. We cleared the necessary
funding hurdles, weathering both CIA intrusiveness and Chinese gov-
ernment reticence. We were on our way.

We decided to make the study as comprehensive as possible. From
the Cancer Atlas, we had access to disease mortality rates on more than

LESSONS FROM CHINA

four dozen different kinds of disease, including individual cancers,
heart diseases and infectious diseases. 6 We gathered data on 367 vari-
ables and then compared each variable with every other variable. We
went into sixty-five counties across China and administered question-
naires and blood tests on 6,500 adults. We took urine samples, directly
measured everything families ate over a three-day period and analyzed
food samples from marketplaces around the country.

The sixty-five counties selected for the study were located in rural
to semi-rural parts of China. This was intentionally done because we
wanted to study people who mostly lived and ate food in the same area
for most of their lives. This was a successful strategy, as we were to learn
than an average of 90-94% of the adult subjects in each county still
lived in the same county where they were born.

When we were done we had more than 8,000 statistically significant
associations between lifestyle, diet and disease variables. We had a
study that was unmatched in terms of comprehensiveness, quality and
uniqueness. We had what the New York Times termed "the Grand Prix of
epidemiology." In short, we had created that revealing snapshot of time
that we had originally envisioned.

This was the perfect opportunity to test the principles that we dis-
covered in the animal experiments. Were the findings in the lab going
to be consistent with the human experience in the real world? Were our
discoveries on aflatoxin-induced liver cancer in rats going to apply to
other types of cancer and other types of diseases in humans?

FOR MORE INFORMATION

We take great pride in the comprehensiveness and quality of the
China Study. To see why, read Appendix B on page 353. You'll find
a more complete discussion of the basic design and characteristics
of the study.

THE CHINESE DIETARY EXPERIENCE

Critical to the importance of the China Study was the nature of the diet
consumed in rural China. It was a rare opportunity to study health-re-
lated effects of a mostly plant-based diet.

In America, 15-16% of our total calories comes from protein and
upwards of 80% of this amount comes from animal-based foods. But in

THE CHINA STUDY

rural China only 9-10% of total calories comes from protein and only
10% of the protein comes from animal-based foods. This means that
there are major nutritional differences in the Chinese and American
diets, as shown in Chart 4.3.

CHART 4.3. CHINESE AND AMERICAN DIETARY INTAKES

Nutrient

China

United States

Calories (kcal/day) 7

2641

1989

Total fat (% of calories)

14.5

34-38

Dietary fiber (g/day)

Total protein (g/day)

Animal protein (% of
calories)

0.8

10-1 1

Total iron (mg/day)

The findings shown in Chart 4.3 are standardized for a body weight
of sixty-five kilograms (143 pounds). This is the standard way that
Chinese authorities record such information and it allows us to easily
compare different populations. (For an American adult male of seventy-
seven kilograms, calorie intake will be about 2,400 calories per day. For
an average rural Chinese adult male of seventy-seven kilograms, calorie
intake will be about 3,000 calories per day.)

In every category seen above, there are massive dietary differences
between the Chinese and American experiences: much higher overall
calorie intake, less fat, less protein, much less animal foods, more fiber
and much more iron are consumed in China. These dietary differences
are supremely important.

While the eating pattern in China is far different from that of the
United States, there is still a lot of variation within China. Experimental
variation (i.e., a range of values) is essential when we investigate diet
and health associations. Fortunately, in the China Study considerable
variation existed for most of the measured factors. There was exception-
al variation in disease rates (Chart 4.2) and more than adequate varia-
tion for clinical measurements and food intakes. For example, blood
cholesterol ranged — as county averages — from highest to lowest almost
twofold, blood beta-carotene about ninefold, blood lipids about three-
fold, fat intake about sixfold and fiber intake about fivefold. This was

LESSONS FROM CHINA

crucial, as we primarily were concerned with comparing each county in
China with every other county.

Ours was the first large study that investigated this particular range
of dietary experience and its health consequences. In effect, we are
comparing, within the Chinese range, diets rich in plant-based foods
to diets very rich in plant-based foods. In almost all other studies, all
of which are Western, scientists are comparing diets rich in animal-
based foods to diets very rich in animal-based foods. The difference
between rural Chinese diets and Western diets, and the ensuing dis-
ease patterns, is enormous. It was this distinction, as much as any
other, that made this study so important.

The media called the China Study a "landmark study." An article in
the Saturday Evening Post said the project "should shake up medical and
nutrition researchers everywhere." 8 Some in the medical establishment
said another study like this could never be done. What I knew was that
our study offered an opportunity to investigate many of the most con-
tentious ideas that I was forming about food and health.

Now, I want to show you what we learned from this study and how
twenty more years of research, thought and experience have changed
not only the way I think about the connection between nutrition and
health, but the way my family and I eat as well.

DISEASES OF POVERTY AND AFFLUENCE

It doesn't take a scientist to figure out that the possibility of death has
been holding pretty steady at 100% for quite some time. There's only
one thing that we have to do in life, and that is to die. I have often met
people who use this fact to justify their ambivalence toward health in-
formation. But I take a different view. I have never pursued health hop-
ing for immortality. Good health is about being able to fully enjoy the
time we do have. It is about being as functional as possible throughout
our entire lives and avoiding crippling, painful and lengthy battles with
disease. There are many better ways to die, and to live.

Because the China Cancer Atlas had mortality rates for more than
four dozen different kinds of disease, we had a rare opportunity to study
the many ways that people die. We wondered: do certain diseases tend
to group together in certain areas of the country? For example, did
colon cancer occur in the same regions as diabetes? If this proved to
be the case, we could assume that diabetes and colon cancer (or other
diseases that grouped together) shared common causes. These causes

THE CHINA STUDY

could include a variety of possibilities, ranging from the geographic
and environmental to the biological. However, because all diseases are
biological processes (gone awry), we can assume that whatever "causes"
are observed, they will eventually operate through biological events.

When these diseases were cross-listed in a way that allowed every
disease rate to be compared with every other disease rate, 9 two groups
of diseases emerged: those typically found in more economically de-
veloped areas (diseases of affluence) and those typically found in rural
agricultural areas (diseases of poverty) 10 (Chart 4.4).

CHART 4.4. DISEASE GROUPINGS OBSERVED IN RURAL CHINA

Diseases of Affluence

(Nutritional Extravagance)

Cancer (colon, lung, breast, leukemia,
childhood brain, stomach, liver), diabe-
tes, coronary heart disease

Diseases of Poverty (Nutritional
inadequacy and poor sanitation)

Pneumonia, intestinal obstruction,
peptic ulcer, digestive disease,
pulmonary tuberculosis, parasitic dis-
ease, rheumatic heart disease, meta-
bolic and endocrine disease other than
diabetes, diseases of pregnancy and
many others

Chart 4.4 shows that each disease, in either list, tends to associate
with diseases in its own list but not in the opposite list. A region in
rural China that has a high rate of pneumonia, for example, will not
have a high rate of breast cancer, but will have a high rate of a parasitic
disease. The disease that kills most Westerners, coronary heart disease,
is more common in areas where breast cancer also is more common.
Coronary heart disease, by the way, is relatively uncommon in many
developing societies of the world. This is not because people die at a
younger age, thus avoiding these Western diseases. These comparisons
are age-standardized rates, meaning that people of the same age are be-
ing compared.

Disease associations of this kind have been known for quite some time.
What the China Study added, however, was an unsurpassed amount of
data on death rates for many different diseases and a unique range of di-
etary experience. As expected, certain diseases do cluster together in the
same geographic areas, implying that they have shared causes.

These two disease groups have usually been referred to as diseases of

LESSONS FROM CHINA

affluence and diseases of poverty. As a developing population accumu-
lates wealth, people change their eating habits, lifestyles and sanitation
systems. As wealth accumulates, more and more people die from "rich"
diseases of affluence than "poor" diseases of poverty Because these dis-
eases of affluence are so tightly linked to eating habits, diseases of afflu-
ence might be better named "diseases of nutritional extravagance." The
vast majority of people in the United States and other Western countries
die from diseases of affluence. For this reason, these diseases are often
referred to as "Western" diseases. Some rural counties had few diseases
of affluence while other counties had far more of these diseases. The
core question of the China Study was this: is it because of differences in
dietary habits?

STATISTICAL SIGNIFICANCE

As I go through this chapter, I will indicate the statistical signifi-
cance of various observations. Roman numeral one (') means 95+%
certainty; roman numeral two (") means 99+% certainty; and ro-
man numeral three ('") means 99.9+% certainty. No roman numeral
means that the association is something less than 95% certainty 1 '
These probabilities also can be described as the probability that an
observation is real. A 95% certainty means a 19 in 20 probability
that the observation is real; a 99% certainty means a 99 in 100 prob-
ability that the observation is real; and a 99.9% certainty means a
999 in 1,000 probability that the observation is real.

BLOOD CHOLESTEROL AND DISEASE

We compared the prevalence of Western diseases in each county with
diet and lifestyle variables and, to our surprise, we found that one of the
strongest predictors of Western diseases was blood cholesterol. 1 "

IN YOUR FOOD— IN YOUR BLOOD

There are two main categories of cholesterol. Dietary cholesterol is
present in the food we eat. It is a component of food, much like sugar,
fat, protein, vitamins and minerals. This cholesterol is found only in
animal-based food and is the one we find on food labels. How much
dietary cholesterol you consume is not something your doctor can
know when he or she checks your cholesterol levels. The doctor can't

THE CHINA STUDY

measure dietary cholesterol any more than he or she can measure how
many hot dogs and chicken breasts you've been eating. Instead, the
doctor measures the amount of cholesterol present in your blood.
This second type of cholesterol, blood cholesterol, is made in the liver.
Blood cholesterol and dietary cholesterol, although chemically identi-
cal, do not represent the same thing. A similar situation occurs with
fat. Dietary fat is the stuff you eat: the grease on your French fries, for
example. Body fat, on the other hand, is the stuff made by your body
and is very different from the fat that you spread on your toast in the
morning (butter or margarine). Dietary fats and cholesterol don't nec-
essarily turn into body fat and blood cholesterol. The way the body
makes body fat and blood cholesterol is extremely complex, involv-
ing hundreds of different chemical reactions and dozens of nutrients.
Because of this complexity, the health effects of eating dietary fat and
dietary cholesterol may be very different from the health effects of
having high blood cholesterol (what your doctor measures) or having
too much body fat.

As blood cholesterol levels in rural China rose in certain counties,
the incidence of "Western" diseases also increased. What made this so
surprising was that Chinese levels were far lower than we had expected.
The average level of blood cholesterol was only 127 mg/dL, which is
almost 100 points less than the American average (215 mg/dL)! 12 Some
counties had average levels as low as 94 mg/dL. For two groups of about
twenty-five women in the inner part of China, average blood cholesterol
was at the amazingly low level of 80 mg/dL.

If you know your own cholesterol levels, you'll appreciate how low
these values really are. In the U.S., our range is around 170-290 mg/dL.
Our low values are near the high values for rural China. Indeed, in the
U.S., there was a myth that there might be health problems if cholesterol
levels were below 150 mg/dL. If we followed that line of thinking, about
85% of the rural Chinese would appear to be in trouble. But the truth is
quite different. Lower blood cholesterol levels are linked to lower rates oj
heart disease, cancer and other Western diseases, even at levels jar below
those considered "safe" in the West.

At the outset of the China Study, no one could or would have pre-
dicted that there would be a relationship between cholesterol and
any of the disease rates. What a surprise we got! As blood cholesterol
levels decreased from 170 mg/dL to 90 mg/dL, cancers of the liver,"
rectum, 1 colon," male lung, 1 female lung, breast, childhood leukemia,

LESSONS FROM CHINA

adult leukemia,' childhood brain, adult brain, 1 stomach and esophagus
(throat) decreased. As you can see, this is a sizable list. Most Americans
know that if you have high cholesterol, you should worry about your
heart, but they don't know that you might want to worry about cancer
as well.

There are several types of blood cholesterol, including LDL and HDL
cholesterol. LDL is the "bad" kind and HDL is the "good" kind. In the
China Study higher levels of the bad LDL cholesterol also were associ-
ated with Western diseases.

Keep in mind that these diseases, by Western standards, were rela-
tively rare in China and that blood cholesterol levels were quite low
by Western standards. Our findings made a convincing case that many
Chinese had an advantage at the lower cholesterol levels, even below
170 mg/dL. Now imagine a country where the inhabitants had blood
cholesterol levels far higher than the Chinese average. You might expect
that these relatively rare diseases, such as heart disease and some can-
cers, would be prevelant, perhaps even the leading killers!

Of course, this is exactly the case in the West. To give a couple of
examples at the time of our study, the death rate from coronary heart
disease was seventeen times higher among American men than rural Chi-
nese men. 13 The American death rate from breast cancer was five times
higher than the rural Chinese rate.

Even more remarkable were the extraordinarily low rates of coronary
heart disease (CHD) in the southwestern Chinese provinces of Sichuan
and Guizhou. During a three-year observation period (1973-1975),
there was not one single person who died of CHD before the age of six-
ty-four, among 246,000 men in a Guizhou county and 181,000 women
in a Sichuan county! 14

After these low cholesterol data were made public, I learned from
three very prominent heart disease researchers and physicians, Drs.
Bill Castelli, Bill Roberts and Caldwell Esselstyn, Jr., that in their long
careers they had never seen a heart disease fatality among their patients
who had blood cholesterol levels below 150 mg/dL. Dr. Castelli was the
long-time director of the famous Framingham Heart Study of NIH; Dr.
Esselstyn was a renowned surgeon at the Cleveland Clinic who did a
remarkable study reversing heart disease (chapter five); Dr. Roberts has
long been editor of the prestigious medical journal Cardiology.

THE CHINA STUDY

BLOOD CHOLESTEROL AND DIET

Blood cholesterol is clearly an important indicator of disease risk. The
big question is: how will food affect blood cholesterol? In brief, animal-
based foods were correlated with increasing blood cholesterol (Chart
4.5). With almost no exceptions, nutrients from plant-based foods were
associated with decreasing levels of blood cholesterol.

Several studies have now shown, in both experimental animals and
in humans, that consuming animal-based protein increases blood cho-
lesterol levels. 15-18 Saturated fat and dietary cholesterol also raise blood
cholesterol, although these nutrients are not as effective at doing this as
is animal protein. In contrast, plant-based foods contain no cholesterol
and, in various other ways, help to decrease the amount of cholesterol
made by the body. All of this was consistent with the findings from the
China Study.

CHART 4.5. FOODS ASSOCIATED WITH BLOOD CHOLESTEROL

As intakes of meat, 1 milk, eggs, fish, 1- " fat 1 and
animal protein go up . . .

Blood Cholesterol goes up.

As intakes of plant-based foods and nutrients (in-
cluding plant protein, 1 dietary fiber," cellulose,"
hemicellulose, 1 soluble carbohydrate," B-vitamins
of plants (carotenes, B 2 , B 3 ),' legumes, light
colored vegetables, fruit, carrots, potatoes and
several cereal grains) go up . . .

Blood Cholesterol goes down.

These disease associations with blood cholesterol were remarkable,
because blood cholesterol and animal-based food consumption both
were so low by American standards. In rural China, animal protein
intake (for the same individual) averages only 7.1 g/day whereas Ameri-
cans average a whopping 70 g/day. To put this into perspective, seven
grams of animal protein is found in about three chicken nuggets from
McDonald's. We expected that when animal protein consumption and
blood cholesterol levels were as low as they are in rural China, there
would be no further association with the Western diseases. But we were
wrong. Even these small amounts of animal-based food in rural China
raised the risk for Western diseases.

We studied dietary effects on the different types of blood cholesterol.
The same dramatic effects were seen. Animal protein consumption by

LESSONS FROM CHINA

men was associated with increasing levels of "bad" blood cholesterol 1 "
whereas plant protein consumption was associated with decreasing lev-
els of this same cholesterol."

Walk into almost any doctor's office and ask which dietary factors af-
fect blood cholesterol levels and he or she will likely mention saturated
fat and dietary cholesterol. In more recent decades, some might also
mention the cholesterol-lowering effect of soy or high-fiber bran prod-
ucts, but few will say that animal protein has anything to do with blood
cholesterol levels.

It has always been this way. While on sabbatical at the University
of Oxford, I attended lectures given to medical students on the dietary
causes of heart disease by one of their prominent professors of medi-
cine. He went on and on about the adverse effects of saturated fat and
cholesterol intakes on coronary heart disease as if these were the only
dietary factors that were important. He was unwilling to concede that
animal protein consumption had anything to do with blood cholesterol
levels, even though the evidence at that time made it abundantly clear
that animal protein was more strongly correlated with blood cholesterol
levels than saturated fat and dietary cholesterol. 15 Like too many others,
his blind faith in the status quo left him unwilling to be open-minded.
As these findings poured in, I was beginning to discover that being
open-minded was not a luxury, but a necessity.

FAT AND BREAST CANCER

If there were some sort of nutrition parade, and each nutrient had a
float, by far the biggest would belong to fat. So many people, from
researchers to educators, from government policy makers to industry
representatives, have investigated or made pronouncements on fat for
so long. People from a huge number of different communities have been
constructing this behemoth for over half a century.

As this strange parade got started on Main Street, USA, the attention
of everyone sitting on the sidewalks would inevitably be drawn to the
fat float. Most people might see the fat float and say, "I should stay away
from that," and then eat a hefty piece of it. Others would climb on the
unsaturated half of the float and say that these fats are healthy and only
saturated fats are bad. Many scientists would point fingers at the fat float
and claim that the heart disease and cancer clowns are hiding inside.
Meanwhile, some self-proclaimed diet gurus, like the late Dr. Robert
Atkins, might set up shop on the float and start selling books. At the

THE CHINA STUDY

end of the day the average person who gorged on the float would be left
scratching his head and feeling queasy, wondering what he should have
done and why.

There's good reason for the average consumer to be confused. The
unanswered questions on fat remain unanswered, as they have for the
past forty years. How much fat can we have in our diets? What kind of
fat? Is polyunsaturated fat better than saturated fat? Is monounsatu-
rated fat better than either? What about those special fats like omega-
3, omega-6, trans fats and DHA? Should we avoid coconut fat? What
about fish oil? Is there something special about flaxseed oil? What's a
high-fat diet anyway? A low-fat diet?

This can be confusing, even for trained scientists. The details that un-
derlie these questions, when considered in isolation, are very misleading.
As you shall see, considering how networks of chemicals behave instead
of isolated single chemicals is far more meaningful.

In some ways, however, it is this foolish mania regarding isolated as-
pects of fat consumption that teaches us the best lessons. Therefore, let's
look a little more closely at this story of fat as it has emerged during the
past forty years. It illustrates why the public is so confused both about
fat and about diet in general.

On average, we consume 35-40% of our total calories as fat. 19 We have
been consuming high-fat diets like this since the late nineteenth century,
at the onset of our industrial revolution. Because we had more money, we
began consuming more meat and dairy, which are relatively high in fat.
We were demonstrating our affluence by consuming such foods.

Then came the mid to late twentieth century when scientists began
to question the advisability of consuming diets so high in fat. National
and international dietary recommendations 20-23 emerged to suggest that
we should decrease our fat intake below 30% of calories. That lasted for
a couple decades, but now, the fears surrounding high-fat diets are abat-
ing. Some authors of popular books even advocate increased fat intake!
Some experienced researchers have suggested that it is not necessary to
go below 30% fat, as long as we consume the right kind of fat.

The level of 30% fat has become a benchmark, even though there is
no evidence to suggest that this is a vital threshold. Let's get some per-
spective on this figure by considering the fat contents of a few foods, as
seen in Chart 4.6.

LESSONS FROM CHINA 83

CHART 4.6: FAT CONTENT OF SAMPLE FOODS

Food

Percent of calories
derived from fat

Butter

100%

McDonald's Double Cheeseburger

67%

Whole Cow's Milk

64%

Ham

61%

Hotdog

54%

Soybeans

42%

"Low-Fat" (or 2%) Milk

35%

Chicken

26%

Spinach

14%

Wheaties Breakfast Cereal

Skim Milk

Peas

Carrots

Green Beans

3.5%

Whole Baked Potatoes

With a few exceptions, animal-based foods contain considerably
more fat than plant-based foods. 24 This is well illustrated by compar-
ing the amount of fat in the diets of different countries. The correlation
between fat intake and animal protein intake is more than 90%. 25 This
means that fat intake increases in parallel with animal protein intake. In
other words, dietary fat is an indicator of how much animal-based food
is in the diet. It is almost a perfect match.

FAT AND A FOCUS ON CANCER

The 1982 National Academy of Sciences (NAS) report on Diet, Nutri-
tion and Cancer, of which 1 was a co-author, was the first expert panel
report that deliberated on the association of dietary fat with cancer.
This report was the first to recommend a maximum fat intake of 30%
of calories for cancer prevention. Previously, the U.S. Senate Select
Committee on Nutrition chaired by Senator George McGovern 26 held
widely publicized hearings on diet and heart disease and recommended
a maximum intake of 30% dietary fat. Although the McGovern report

THE CHINA STUDY

generated a public discourse on diet and disease, it was the 1982 NAS
report that gave momentum to this debate. Its focus on cancer, as op-
posed to heart disease, increased public interest and concern. It spurred
additional research activity and public awareness of the importance of
diet in disease prevention.

Many of the reports at the time 20, 11 - 28 were centered on the question of
how much dietary fat was appropriate for good health. The unique atten-
tion given to fat was motivated by international studies showing that the
amount of dietary fat consumed was closely associated with the incidence
of breast cancer, large bowel cancer and heart disease. These were the
diseases that kill the majority of people in Western countries before their
time. Clearly, this correlation was destined to attract great public atten-
tion. The China Study was begun in the midst of this environment.

The best known study, 29 in my view, was that of the late Ken Carroll,
professor at the University of Western Ontario in Canada. His findings
showed a very impressive relationship between dietary fat and breast
cancer (Chart 4.7).

This finding, which corresponded to the earlier reports of others, 3 - 30
became especially intriguing when compared with migrant studies. 31,32
These studies showed that people who migrated from one area to an-
other and who started eating the typical diet of their new residency as-
sumed the disease risk of the area to which they moved. This strongly

CHART 4.7: TOTAL FAT INTAKE AND BREAST CANCER

o
o
o
o~
o

25 -I

15 -

10 -

FEMALE

• NETHERLANDS

• UK • DENMARK
CANADA « • NEW ZEALAND
• SWITZERLAND
IRELAND** AUS

BELGIUM

AUSTRALIA •

AUSTRIA •

• SWEDEN
-•GERMANY

• ITALY

• CZECH
• • FINLAND

• PORTUGAL HUNGARY

HONGKONG q POLAND

VENEZUELA^ V« w ,gg
PANAMA •viifinsiAuiA "" c "- c

NORWAY • FRANCE

' YUGOSLAVIA

PHILIPPINES

COLOMBIA

'PUERTO RICO

. # • MEXICO

JAPAN • TAIWAN

THAILAND

• •

• CEYLON
EL SALVADOR

— I

- 1 —

~l —

100

— 1 —

120

- 1 —

140

160

~I —
180

Total Dietary Fat Intake (g/day)

LESSONS FROM CHINA

implied that diet and lifestyle were the principle causes of these dis-
eases. It also suggested that genes are not necessarily that important.
As noted earlier, a very prominent report by Sir Richard Doll and Sir
Richard Peto of the University of Oxford (U.K.) submitted to the U.S.
Congress summarized many of these studies and concluded that only
2-3% of all cancers could be attributed to genes. 4

Do the data from these international and migrant studies mean
that we can lower our rate of breast cancer to almost zero if we make
perfect lifestyle choices? The information certainly suggests that this
could be the case. Concerning the evidence in Chart 4.7, the solution
seems obvious: if we eat less fat, then we'll lower our breast cancer risk.
Most scientists made this conclusion and some surmised that dietary
fat caused breast cancer. But that interpretation was too simple. Other
charts prepared by Professor Carroll were largely, almost totally, ignored
(Charts 4.8 and 4.9). They show that breast cancer was associated with
animal fat intake but not with plant fat.

In rural China, dietary fat intake (at the time of the survey in 1983)
was very different from the United States in two ways. First, fat was only
14.5% of calorie intake in China, compared with about 36% in the U.S.
Second, the amount of fat in the diets of rural China depended almost
entirely on the amount of animal-based food in the diet, just like the

CHART 4.8: ANIMAL FAT INTAKE AND BREAST CANCER

FEMALE f NETHERLANDS

#UK DENMARK

SWITZERLAND. CANADA* • NEW ZEALAND

>WII£CKLAI1U # IREL AND

o20
o
o

Q 10

9 IRELAND

BELGIUM* # US

^SWEDEN • AUSTRALIA
GERMANY • •alalia

• f NORWAY

15 - • ITALY AUSTRIA •FRANCE

• CZECH

•PORTUGAL • ^FINLAND

HUNGARY

HONG KONG
BULGARIA • • POLAND

VENEZUEUy^ R E 0MAN|A

PANAMA GREECETplLYUGOSLAVIA
< s J PHILIPPINES • COLOMBIA • PUERTO RICO
JAPAN*.* MEXICO
CEYLON • TAIWAN
• THAILAND

• • EL SALVADOR

1 1 1 1 1 1 1 r

20 40 60 80 100 120 140 160 180

Animal Fat Intake (g/day)

THE CHINA STUDY

25 -i

CHART 4.9: PLANT FAT INTAKE AND BREAST CANCER

FEMALE

• NETHERLANDS

DENMARK
"CANADA

IRELAND BELGIUM*

20 -

J 15-

NEW ZEALAND

► SWITZERLAND

> AUSTRALIA
NORWAY (

USA
0 SWEDEN
AUSTRIA* • GERMANY

'FRANCE,

1 CZECHOSLOVAKIA

• ITALY

FINLAND* •HUNGARY

POLAND* HONGKONG

• PORTUGAL

rune* * wBULGARIA
ROMANIA© VENEZUELA
ROMANIA* • PANAMA

PUERTO RICO

YUGOSLAVIA
PHILIPPINES* 'COLOMBIA
TAIWAN* • JAPAN

• SPAIN
'GREECE

MEXICO
• CEYLON

THAILAND <

• EL SALVADOR

—r

30 40 50

Vegetable Fat Intake (g/day)

findings in Chart 4.7. The correlation between dietary fat and animal
protein in rural China was very high, at 70-84%, 33 similar to the 93%
seen when comparing different countries. 25

This is important because in China and the international studies, fat
consumption was only an indication of animal-based food consumption.
Thus, the association between fat and breast cancer might really be tell-
ing us that as consumption of animal-based foods goes up, so does breast
cancer. This is not the case in the U.S., where we selectively add or re-
move fat from our foods and our diets. We get as much or more fat from
plant-based food (potato chips, French fries) as we get from processed
animal-based foods (skim milk, lean cuts of meat). China does not tin-
ker with fat in their food supply as we do here.

At this very low range of dietary fat in China, from 6%-24%, I ini-
tially thought that dietary fat would not be linked with diseases like
heart disease or the various cancers, as it is in the West. Some people
in the U.S. — like many of my colleagues in science and medicine — call
a 30% fat diet a "low-fat" diet. Therefore, a low-fat diet containing only

LESSONS FROM CHINA

25-30% fat was thought to be low enough to obtain the maximum
amount of health benefits. This implied that going lower provided no
further benefit. Surprise!

Findings from rural China showed that reducing dietary fat from
24% to 6% was associated with lower breast cancer risk. However, lower
dietary fat in rural China meant less consumption not only of fat but,
more importantly, of animal-based food.

This connection of breast cancer with dietary fat, thus with animal-
based foods, brought into consideration other factors that also place a
woman at risk for breast cancer:

• Early age of menarche (age of first menstruation)

• High blood cholesterol

• Late menopause

• High exposure to female hormones

What does the China Study show regarding these risk factors? Higher
dietary fat is associated with higher blood cholesterol 1 and both of these
factors, along with higher female hormone levels, are associated, in
turn, with more breast cancer 1 and earlier age of menarche. 1

The much later age of menarche in rural China is remarkable. Twen-
ty-five women in each of the 130 villages in the survey were asked when
they had their first menstrual period. The range of village averages was
fifteen to nineteen years, with an average of seventeen years. The U.S.
average is roughly eleven years!

Many studies have shown that earlier menarche leads to higher risk for
breast cancer. 34 Menarche is triggered by the growth rate of the girl; the
faster the growth, the earlier the age of onset. It also is well established
that rapid growth of young girls often leads to greater adult body height
and more body weight and body fatness, each of which is associated with
higher breast cancer risk. Early age of menarche, both in Chinese and in
Western women, also leads to higher levels of blood hormones such as
estrogen. These hormone levels remain high throughout the reproductive
years if consumption of a diet rich in animal-based food is maintained.
Under these conditions, age of menopause is deferred by three to four
years, 1 thus extending the reproductive life from beginning to end by
about nine to ten years and greatly increasing lifetime exposure to female
hormones. Other studies have shown that an increase in years of repro-
ductive life is associated with increased breast cancer risk. 33 ' 36

This network of relationships becomes still more impressive. Higher

THE CHINA STUDY

fat consumption is associated with higher blood levels of estrogen dur-
ing the critical years of thirty-five to forty-four years'" and higher blood
levels of the female hormone prolactin during the later years of fifty-five
to sixty-four years." 1 These hormones are highly correlated with animal
protein intake 1 " and milk" 1 and meat." Unfortunately we could not dem-
onstrate whether these hormone levels were directly related to breast
cancer risk in China because the rate of disease is so low. 37

Nonetheless, when hormone levels among Chinese women were com-
pared with those of British women, 38 Chinese estrogen levels were only
about one-half those of the British women, who have an equivalent hor-
mone profile to that of American women. Because the length of the repro-
ductive life of a Chinese woman is only about 75% of that of the British
(or American) woman, this means that with lower estrogen levels, the
Chinese woman only experiences about 35-40% of the lifetime estrogen
exposure of British (and American) women. This corresponds to Chinese
breast cancer rates that are only one-fifth of those of Western women.

The strong association of a high-animal protein, high-fat diet with
reproductive hormones and early age of menarche, both of which raise
the risk of breast cancer, is an important observation. It makes clear that
we should not have our children consume diets high in animal-based
foods. If you are a woman, would you ever have imagined that eating
diets higher in animal-based foods would expand your reproductive life
by about nine to ten years? As an aside, an interesting implication of
this observation, as noted by Ms. magazine founder Gloria Steinem, is
that eating the right foods could reduce teenage pregnancy by delaying
the age of menarche.

Beyond the hormone findings, is there a way to show that animal-
based food intake relates to overall cancer rates? This is somewhat dif-
ficult, but one of the factors we measured was how much cancer there
was in each family Animal protein intake was convincingly associated
in the China Study with the prevalence of cancer in families." 1 This as-
sociation is an impressive and significant observation, considering the
unusually low intake of animal protein.

Diet and disease factors such as animal protein consumption or
breast cancer incidence lead to changes in the concentrations of cer-
tain chemicals in our blood. These chemicals are called biomarkers.
As an example, blood cholesterol is a biomarker for heart disease. We
measured six blood biomarkers that are associated with animal protein
intake. 39 Do they confirm the finding that animal protein intake is asso-

LESSONS FROM CHINA

ciated with cancer in families? Absolutely. Every single animal protein-
related blood biomarker is significantly associated with the amount of
cancer in a family."" 11 '

In this case, multiple observations, tightly networked into a web,
show that animal-based foods are strongly linked to breast cancer. What
makes this conclusion especially compelling are two kinds of evidence.
First, the individual parts of this web were consistently correlated and,
in most cases, were statistically significant. Second, this effect occurred
at unusually low intakes of animal-based foods.

Our investigation of breast cancer (detailed further in chapter seven)
is a perfect example of what makes the China Study so convincing.
Rather than a single, simple association of fat and breast cancer, 1 we were
able to construct a much more expansive web of information about how
diet affects breast cancer risk. We were able to examine in multiple ways
the role of diet and cholesterol, age of menarche and female hormone
levels, all of which are known risk factors for breast cancer. When each
new finding pointed in the same direction, we were able to see a picture
that was convincing, consistent and biologically plausible.

THE IMPORTANCE OF FIBER

The late Professor Denis Burkitt, of Trinity College, Dublin, was un-
usually articulate. His common sense, scientific credibility and sense
of humor made quite an impression on me when I first met him at a
Cornell seminar. The subject of his work was dietary fiber. He had trav-
eled 10,000 miles in a jeep over rugged countryside to study the dietary
habits of Africans.

He asserted that even though fiber was not digested, it was vital for
good health. Fiber was able to pull water from the body into the intestines
to keep things moving along. These undigested fibers, like stick-um pa-
per, also gather up nasty chemicals that find their way into our intestines
and that might be carcinogenic. If we don't consume enough fiber, we are
susceptible to constipation-based diseases. According to Burkitt, these in-
clude large bowel cancer, diverticulosis, hemorrhoids and varicose veins.

In 1993, Dr. Burkitt was awarded the prestigious Bower Award, the
richest award in the world next to the Nobel Prize. He invited me to
speak at his award ceremony at the Franklin Institute in Philadelphia,
only two months before his unfortunate passing. He offered his opinion
that our China Study was the most significant work on diet and health
in the world at that time.

THE CHINA STUDY

Dietary fiber is exclusively found in plant-based foods. This mate-
rial, which gives rigidity to the cell walls of plants, comes in thousands
of different chemical variations. It is mostly made of highly complex
carbohydrate molecules. We digest very little or no fiber. Nonetheless,
fiber, having few or no calories itself, helps dilute the caloric density of
our diets, creates a sense of fullness and helps to shut down appetite,
among other things. In doing so, it satisfies our hunger and minimizes
the overconsumption of calories.

Average fiber intake (Chart 4. 10) is about three times higher in China
than in the U.S. 40 These differences are exceptional, especially consider-
ing the fact that many county averages were even much higher.

But according to some "experts" in the U.S., there is a dark side to
dietary fiber. They contend that if fiber intake is too high our bodies
are not able to absorb as much iron and related minerals, which are
essential for health. The fiber may bind with these nutrients and carry
them through our system before we are able to digest them. They say
that the maximum level of fiber intake should be around thirty to thirty-
five grams per day, which is only about the average intake of the rural
Chinese.

We studied this iron/fiber issue very carefully in the China Study. As
it turns out, fiber is not the enemy of iron absorption as so many experts
claim it to be. We measured how much iron the Chinese were consum-
ing and how much was in their bodies. Iron was measured in six differ-
ent ways (four blood biomarkers and two estimates of iron intake) and

CHART 4.10: AVERAGE INTAKES OF DIETARY FIBER, GM/DAY

China United States

LESSONS FROM CHINA

when we compared these measurements with fiber intake, there was no
evidence showing that increasing fiber intake impaired iron absorption in
the body. In fact, we found the opposite effect. A good indicator of how
much iron is in the blood, hemoglobin, actually increased with greater
intakes of dietary fiber. 1 As it turns out, high-fiber foods, like wheat
and corn (but not the polished rice consumed in China) also happen to
be high in iron, meaning that the higher the consumption of fiber, the
higher the consumption of iron." 1 Iron intake in rural China (34 mg/
day) was surprisingly high when compared to the average American in-
take (18 mg/day) and it was far more associated with plant-based foods
than with animal-based foods. 41

The China findings on dietary fiber and iron, like so many other ob-
servations in this study, did not support the common view of Western
scientists. People who consume more plant-based foods, thus more di-
etary fiber, also consume more iron," 1 all of which results in statistically
significant higher levels of hemoglobin. Unfortunately, a bit of confu-
sion has arisen over the fact that some people in rural China, including
women and children, have low iron levels. This is especially true in
areas where parasitic diseases are more common. In areas of rural China
where parasitic diseases were more common, iron status was lower. 1
This has given some the opportunity to claim that these people need
more meat, but the evidence indicates that the problem would be much
better corrected by reducing parasitism in these areas.

Much of the initial interest in dietary fiber arose with Burkitt's travels
in Africa and his claim that large bowel cancer is lower among popula-
tions who consume high-fiber diets. Burkitt made this claim popular
but the story is at least 200 years old. In England during the late eigh-
teenth century and early nineteenth century, it was claimed by some of
the leading physicians that constipation, which was associated with less
bulky diets (i.e., low-fiber diets), was associated with a higher risk of
cancer (usually breast and "intestinal" cancers).

At the beginning of the China Study, this belief that fiber might pre-
vent large bowel cancer was the prevailing view, although the 1982 Na-
tional Academy of Sciences Committee on Diet, Nutrition and Cancer,
"found no conclusive evidence to indicate that dietary fiber . . . exerts a
protective effect against colorectal cancer in humans." The report went
on to conclude, "... if there is such an effect, specific components of
fiber, rather than total dietary fiber, are more likely to be responsible." 20
In hindsight, our discussion of this issue was inadequate. The question,

THE CHINA STUDY

the review of the research literature and the interpretation of the evi-
dence were too focused on looking for a specific fiber as the responsible
cause. Finding none, the fiber hypothesis was dismissed.

It was a mistake. The China Study provided evidence that there is
a link with certain cancers. The results showed that high-fiber intake
was consistently associated with lower rates of cancers of the rectum
and colon. High-fiber intakes also were associated with lower levels of
blood cholesterol. 1 " Of course, high-fiber consumption reflected high
plant-based food consumption; foods such as beans, leafy vegetables
and whole grains are all high in fiber.

ANTIOXIDANTS, A BEAUTIFUL COLLECTION

One of the more obvious characteristics of plants is their wide range
of bright colors. If you admire how food is presented, it's hard to beat
a plate of fruits and vegetables. The reds, greens, yellows, purples and
oranges of plant foods are tempting and very healthy. This link between
nicely colored vegetables and their exceptional health benefits has often
been noted. It turns out that there is a beautiful, scientifically sound
story behind this color/health link.

The colors of fruits and vegetables are derived from a variety of chem-
icals called antioxidants. These chemicals are almost exclusively found
in plants. They are only present in animal-based foods to the extent that
animals eat them and store a small amount in their own tissues.

Living plants illustrate nature's beauty, both in color and in chemis-
try. They take the energy of the sun and transform it into life through
the process of photosynthesis. In this process, the sun's energy is first
turned into simple sugars, and then into more complex carbohydrates,
fats and proteins.

This complex process amounts to some pretty high-powered activity
within the plant, all of which is driven by the exchange of electrons be-
tween molecules. Electrons are the medium of energy transfer. The site
at which photosynthesis takes place is a bit like a nuclear reactor. The
electrons zooming around in the plant that are changing the sunlight
into chemical energy must be managed very carefully. If they stray from
their rightful places in the process, they may create free radicals, which
can wreak havoc in the plant. It would be like the core of a nuclear reac-
tor leaking radioactive materials (free radicals) that can be very danger-
ous to the surrounding area.

So how does the plant manage these complex reactions and protect

LESSONS FROM CHINA

against errant electrons and free radicals? It puts up a shield around
potentially dangerous reactions that sponges up these highly reactive
substances. The shield is made up of antioxidants that intercept and
scavenge electrons that might otherwise stray from their course.

Antioxidants are usually colored because the same chemical property
that sponges up excess electrons also creates visible colors. Some of
these antioxidants are called carotenoids, of which there are hundreds.
They vary in color from the yellow color of beta-carotene (squash), to
the red color of lycopene (tomatoes), to the orange color of the odd-
sounding crytoxanthins (oranges). Other antioxidants may be colorless
and these include chemicals such as ascorbic acid (vitamin C) and vita-
min E, which act as antioxidants in other parts of plants that need to be
protected from the hazards of wayward electrons.

What makes this remarkable process relevant for us animals, howev-
er, is that we produce low levels of free radicals throughout our lifetime.
Simply being exposed to the sun's rays, to certain industrial pollutants
and to improperly balanced nutrient intakes creates a background of
unwanted free radical damage. Free radicals are nasty. They can cause
our tissues to become rigid and limited in their function. It is a bit like
old age, when our bodies become creaky and stiff. To a great extent, this
is what aging is. This uncontrolled free radical damage also is part of the
processes that give rise to cataracts, to hardening of the arteries, to can-
cer, to emphysema, to arthritis and many other ailments that become
more common with age.

But here's the kicker: we do not naturally build shields to protect
ourselves against free radicals. As we are not plants, we do not carry
out photosynthesis and therefore do not produce any of our own anti-
oxidants. Fortunately the antioxidants in plants work in our bodies the
same way they work in plants. It is a wonderful harmony. The plants
make the antioxidant shields, and at the same time make them look in-
credibly appealing with beautiful, appetizing colors. Then we animals,
in turn, are attracted to the plants and eat them and borrow their antiox-
idant shields for our own health. Whether you believe in God, evolution
or just coincidence, you must admit that this is a beautiful, almost spiri-
tual, example of nature's wisdom.

In the China Study, we assessed antioxidant status by recording the
intakes of vitamin C and beta-carotene and measuring the blood levels
of vitamin C, vitamin E and carotenoids. Among these antioxidant bio-
markers, vitamin C provided the most impressive evidence.

THE CHINA STUDY

The most significant vitamin C association with cancer was its re-
lationship with the number of cancer-prone families in each area. 42
When levels of vitamin C in the blood were low, these families were
more likely to have a high incidence of cancer. 1 " Low vitamin C was
prominently associated with higher risk for esophageal cancer," 1 for
leukemia and cancers of the nasopharynx, breast, stomach, liver,
rectum, colon and lung. It was esophageal cancer that first attracted
NOVA television program producers to report on cancer mortality in
China. It was this television program that spurred our own survey
to see what was behind this story. Vitamin C primarily comes from
fruit, and eating fruit was also inversely associated with esophageal
cancer." 43 Cancer rates were five to eight times higher for areas where
fruit intake was lowest. The same vitamin C effect existing for these
cancers also existed for coronary heart disease, hypertensive heart dis-
ease and stroke." Vitamin C intake from fruits clearly showed a power-
ful protective effect against a variety of diseases.

The other measures of antioxidants, blood levels of alpha and beta-
carotene (a vitamin precursor) and alpha and gamma tocopherol (vita-
min E) are poor indicators of the effects of antioxidants. These antioxi-
dants are transported in the blood by lipoprotein, which is the carrier of
"bad" cholesterol. So anytime we measured these antioxidants, we were
simultaneously measuring unhealthy biomarkers. This was an experi-
mental compromise that diminished our ability to detect the beneficial
effects of the carotenoids and the tocopherols, even when these benefits
are known to exist. 44 We did, however, find that stomach cancer was
higher when the blood levels of beta-carotene were lower. 45

Can we say that vitamin C, beta-carotene and dietary fiber are solely
responsible for preventing these cancers? In other words, can a pill con-
taining vitamin C and beta-carotene or a fiber supplement create these
health effects? No. The triumph of health lies not in the individual nu-
trients, but in the whole foods that contain those nutrients: plant-based
foods. In a bowl of spinach salad, for example, we have fiber, antioxi-
dants and countless other nutrients that are orchestrating a wondrous
symphony of health as they work in concert within our bodies. The
message could not be simpler: eat as many whole fruits, vegetables and
whole grains as you can, and you will probably derive all of the benefits
noted above as well as many others.

I have been making this point about the health value of whole plant-
based foods ever since vitamin supplements were introduced on a large

LESSONS FROM CHINA

scale in the marketplace. And 1 have watched in dismay how the indus-
try and the media convinced so many Americans that these products
represent the same good nutrition as do whole, plant-based foods. As
we shall see in the later chapters, the promised health benefits of tak-
ing single-nutrient supplements are proving to be highly questionable.
The "take-home message": if you want vitamin C or beta-carotene, don't
reach for the pill bottle — reach for the fruit or leafy green vegetables.

THE ATKINS CRISIS

In case you haven't noticed, there is an elephant in the room. It goes by
the name "low-carb diet," and it has become very popular. Almost all
diet books on store shelves are variations of this one theme: eat as much
protein, meat and fat as you want, but stay away from those "fatty"
carbs. As you have seen already in this book, my research findings and
my point of view show that eating this way is perhaps the single great-
est threat to American health we currently face. So what is the story,
anyway?

One of the fundamental arguments at the beginning of most low-
carbohydrate, high-protein diet books is that America has been wallow-
ing in low-fat mania at the advice of experts for the past twenty years,
yet people are fatter than ever. This argument has an intuitive appeal,
but there is one inconvenient fact that is consistently ignored: accord-
ing to a report 46 summarizing government food statistics, "Americans
consumed thirteen pounds [my emphasis] more [added] fats and oils
per person in 1997 than in 1970, up from 52.6 to 65.6 pounds." It is
true that we have had a trend to consuming fewer of our total calories
as fat, when considered as a percentage, but that's only because we have
outpaced our gorging on fat by gorging on sugary junk food. Simply by
looking at the numbers, anybody can see that America has not adopted
the "low-fat" experiment — not by any stretch of the imagination.

In fact, the claim that the low-fat "brainwashing" experiment has
been tried and failed is often the first of many statements of fact in
current diet books that can be described either as severe ignorance or
opportunistic deceit. It is difficult to know where to begin to refute the
maze of misinformation and false promises commonly made by authors
completely untrained in nutrition, authors who have never conducted
any peer-reviewed, professionally based experimental research. And
yet these books are immensely popular. Why? Because people do lose
weight, at least in the short term.

THE CHINA STUDY

In one published study 47 funded by the Atkins Center for Comple-
mentary Medicine, researchers put fifty-one obese people on the Atkins
diet. 48 The forty-one subjects who maintained the diet over the course
of six months lost an average of twenty pounds. In addition, average
blood cholesterol levels decreased slightly, 47 which was perhaps even
more important. Because of these two results, this study was presented
in the media as real, scientific proof that the Atkins diet works and is
safe. Unfortunately, the media didn't go much deeper than that.

The first sign that all is not rosy is that these obese subjects were
severely restricting their calorie intake during the study. The average
American consumes about 2,250 calories per day. 49 When the study
participants were on the diet, they consumed an average of 1,450 calo-
ries per day. That's 35% fewer calories! I don't care if you eat worms
and cardboard; if you eat 35% fewer calories, you will lose weight and
your cholesterol levels will improve 50 in the short run, but that is not to
say that worms and cardboard form a healthy diet. One may argue that
those 1,450 calories are so satisfying that people feel full on this diet,
but if you compare calorie input and calorie expenditure, it's a matter
of simple math that a person cannot sustain this amount of calorie re-
striction over a period of years or decades without either becoming an
invalid or melting away into nothing. People are notoriously unsuccess-
ful at significantly restricting their energy intake over any long period of
time, and that is why there has yet to be a long-term study that shows
success with the "low-carb" diets. This, however, is only the beginning
of the problems.

In this same study, funded by the Atkins group, researchers report,
"At some point during the twenty-four weeks, twenty-eight subjects
(68%) reported constipation, twenty-six (63%) reported bad breath,
twenty-one (51%) reported headache, four (10%) noted hair loss, and
one woman (1%) reported increased menstrual bleeding." 47 They also
refer to other research, saying, "Adverse effects of this diet in children
have included calcium oxalate and urate kidney stones . . . vomiting,
amenorrhea [when a girl misses her period], hypercholesterolemia
[high cholesterol] and ... vitamin deficiencies (ref. cited)." 47 Addition-
ally, they found that the dieters had a stunning 53% increase in the
amount of calcium they excreted in their urine, 47 which may spell di-
saster for their bone health. The weight loss, some of which is simply
initial fluid loss, 51 may come with a very high price.

A different review of low-carbohydrate diets published by research-

LESSONS FROM CHINA

ers in Australia concludes, "Complications such as heart arrhythmias,
cardiac contractile function impairment, sudden death, osteoporosis,
kidney damage, increased cancer risk, impairment of physical activity
and lipid abnormalities can all be linked to long-term restriction of car-
bohydrates in the diet." 51 One teenage girl recently died suddenly after
being on a high-protein diet. 52,53 In short, most people will be unable to
maintain this diet for the rest of their lives, and even if anybody man-
ages to do so, they may be asking for serious health problems down the
road. I have heard one doctor call high-protein, high-fat, low-carbohy-
drate diets "make-yourself-sick" diets, and 1 think that's an appropri-
ate moniker. You can also lose weight by undergoing chemotherapy or
starting a heroin addiction, but I wouldn't recommend those, either.

One final thought: the diet is not all that Atkins recommends. Indeed,
most diet books are merely one part of huge food and health empires.
In the case of the Atkins diet, Dr. Atkins states that many of his patients
require nutrient supplements, some of which are used to combat "com-
mon dieters' problems." 54 In one passage, after making unsubstantiated
claims about the efficacy of antioxidant supplements that contradict
recent studies, 55 he writes, "Add to the [antioxidants] the vita-nutri-
ents known to be useful for each of the myriad medical problems my
patients face, and you'll see why many of them take over thirty vitamin
pills a day." 56 Thirty pills a day?

There are snake oil salesmen, who have no professional research,
professional training or professional publications in the field of nutri-
tion, and there are scientists, who have formal training, have conducted
research and have reported on their findings in professional forums.
Perhaps it is a testament to the power of modern marketing savvy that
an obese man with heart disease and high blood pressure 57 became one
of the richest snake oil salesmen ever to live, selling a diet that promises
to help you lose weight, to keep your heart healthy and to normalize
your blood pressure.

THE TRUTH ABOUT CARBOHYDRATES

An unfortunate outcome of the recent popularity of diet books is that
people are more confused than ever about the health value of carbo-
hydrates. As you will see in this book, there is a mountain of scientific
evidence to show that the healthiest diet you can possibly consume is
a high-carbohydrate diet. It has been shown to reverse heart disease,
reverse diabetes, prevent a plethora of chronic diseases, and yes, it has

THE CHINA STUDY

been shown many times to cause significant weight loss. But it's not
quite as simple as that.

At least 99% of the carbohydrates that we consume are derived from
fruits, vegetables and grains. When these foods are consumed in the
unprocessed, unrefined and natural state, a large proportion of the car-
bohydrates are in the so-called "complex" form. This means that they
are broken down in a controlled, regulated manner during digestion.
This category of carbohydrates includes the many forms of dietary fiber,
almost all of which remain undigested — but still provide substantial
health benefits. In addition, these complex carbohydrates from whole
foods are packaged with generous amounts of vitamins, minerals and
accessible energy. Fruits, vegetables and whole grains are the healthiest
foods you can consume, and they are primarily made of carbohydrates.

On the opposite side of the spectrum, there are highly processed, high-
ly refined carbohydrates that have been stripped of their fiber, vitamins
and minerals. Typical simple carbohydrates are found in foods like white
bread, processed snack items including crackers and chips made with
white flour, sweets including pastries and candy bars and sugar-laden soft
drinks. These highly refined carbohydrates originate from grains or sugar
plants, like sugar cane or the sugar beet. They are readily broken down
during digestion to the simplest form of the carbohydrates, which are
absorbed into the body to give blood sugar, or glucose.

Unfortunately, most Americans consume voluminous amounts of
simple, refined carbohydrates and paltry amounts of complex carbo-
hydrates. For example, in 1996, 42% of Americans ate cakes, cookies,
pastries or pies on any given day, while only 10% ate any dark green
vegetables. 46 In another ominous sign, only three vegetables accounted
for half of the total vegetable servings in 1996 46 : potatoes, which were
mostly consumed as fries and chips; head lettuce, one of the least nutri-
ent-dense vegetables you can consume, and canned tomatoes, which is
probably only a reflection of pizza and pasta consumption. Add to that
the fact that the average American consumed thirty-two teaspoons of
added sugars per day in 1996,* 6 and it's clear that Americans are gorging
almost exclusively on refined, simple carbohydrates, at the exclusion of
healthful complex carbohydrates.

This is bad news, and this, in large measure, is why carbohydrates as
a whole have gotten such a bad rap; the vast majority of carbohydrates
consumed in America are found in junk food or grains so refined that
they have to be supplemented with vitamins and minerals. On this

LESSONS FROM CHINA

point, the popular diet authors and I agree. For example, you could eat
a low-fat, high-carbohydrate diet by exclusively eating the following
foods: pasta made from refined flour, baked potato chips, soda, sugary
cereals and low-fat candy bars. Eating this way is a bad idea. You will
not derive the health benefits of a plant-based diet eating these foods. In
experimental research, the health benefits of a high-carbohydrate diet
come from eating the complex carbohydrates found in whole grains,
fruits and vegetables. Eat an apple, a zucchini or a plate of brown rice
topped with beans and other vegetables.

THE CHINA STUDY WEIGHS IN

With regard to weight loss, there are some surprising findings from the
China Study that shed light on the weight loss debate. When we started
the China Study, I thought that China had the opposite problem from
that of the U.S. 1 had heard that China could not feed itself, that it was
prone to famines and that there was not enough food for people to at-
tain their full adult height. Very simply, there were not enough calories
to go around. Although China has, during the last fifty years, had its
share of nutritional problems, we were to learn that these views on calo-
rie intake were dead wrong.

We wanted to compare the calorie consumption in China and
America, but there was a catch. Chinese are more physically active than
Americans, especially in rural areas, where manual labor is the norm. To
compare an extremely active laborer with an average American would
be misleading. It would be like comparing the amount of energy con-
sumed by a manual laborer at hard work with the amount of energy
consumed by an accountant. The vast difference in calorie intake sure
to exist between these individuals would tell us nothing of value and
only confirm that the manual laborer is more active.

To overcome this problem, we ranked the Chinese into five groups
according to their levels of physical activity. After figuring out the calo-
rie intakes of the least active Chinese, the equivalent of office workers,
we then compared their calorie intake with the average American. What
we found was astonishing.

Average calorie intake, per kilogram of body weight, was 30% higher
among the least active Chinese than among average Americans. Yet,
body weight was 20% lower (Chart 4.11). How can it be that even the
least active Chinese consume more calories yet have no overweight
problems? What is their secret?

100

THE CHINA STUDY

CHART 4.1 1: CALORIE CONSUMPTION (KCAL/KG)
AND BODY WEIGHT

Calorie Intake (kcal/kg) Average Body Mass Index

There are two possible explanations for this apparent paradox. First,
even the Chinese office workers are more physically active than aver-
age Americans. Anyone familiar with China knows that many office
workers travel on bicycles. Thus, they consume more calories. Even so,
we cannot tell how much of the extra calorie consumption was due to
physical activity and how much to something else, perhaps their food.

We do know, however, that some people use the calories they con-
sume differently from other people. We often say that "they have a
higher rate of metabolism" or "it's in their genes." You know these
people. They are the ones who seem to eat all they want and still not
gain weight. Then there are most of us, who need to watch our calorie
intake — or so we think. This is the simplistic interpretation.

I have a more comprehensive interpretation that is based on our own
considerable research and on the studies of others. It goes like this.
Provided that we aren't restricting our calorie intake, those of us who
consume a high-fat, high-protein diet simply retain more calories than
we need. We store these calories as body fat, perhaps weave it into our
muscle fibers (we call it "marbling" in beef animals) and perhaps store
it in the more obvious places, like our butt, our midsection or around
our face and upper thighs.

Here's the clincher: only a small amount of calories needs to be re-
tained by our body to cause significant change in body weight. For ex-
ample, if we retain only an extra fifty calories per day this can lead to an
extra ten pounds per year. You may not think that this is a lot, but over
a period of five years, that's an extra fifty pounds.

Some people would hear this and might be inclined to just eat fifty
fewer calories per day. This, theoretically, could make a difference, but it

LESSONS FROM CHINA

101

is entirely impractical. It is impossible to keep track of daily calorie in-
take with such precision. Think about eating a meal at a restaurant. Do
you know how many calories each meal has? What about the casserole
you might fix? What about the steak you might buy? Do you know the
number of calories they contain? Of course not.

The truth is this: despite any short-term caloric restriction regimes
we may follow, our body through many mechanisms, will ultimately
choose how many calories to take in and what to do with them. Our at-
tempts to limit calorie intake is short-lived and imprecise, whether we
do it by limiting carbohydrates or fat.

The body employs a delicate balancing act and some very intricate
mechanisms in deciding how to use the calories being consumed.
When we treat our body well by eating the right foods, it knows how
to partition the calories away from body fat and into the more desirable
functions like keeping the body warm, running the body metabolism,
supporting and encouraging physical activity or just disposing of any
excess. The body is using multiple intricate mechanisms to decide how
calories get used, stored or "burned off."

Consuming diets high in protein and fat transfers calories away from
their conversion into body heat to their storage form — as body fat
(unless severe calorie restriction is causing weight loss). In contrast,
diets low in protein and fat cause calories to be "lost" as body heat. In
research, we say that storing more calories as fat and losing less as heat
means being more efficient. I bet that you would rather be a little more
inefficient and convert it into body heat rather than body fat, right?
Well, simply consuming a diet lower in fat and protein can do this.

This is what our China Study data show Chinese consume more
calories both because they are more physically active and because their
consumption of low-fat, low-protein diets shifts conversion of these
calories away from body fat to body heat. This is true even for the least
physically active Chinese. Remember, it takes very little, only fifty calo-
ries a day, to change our storage of body fat and thus change our body
weight. 58

We saw the same phenomenon in our experimental animals fed the
low-protein diets. They routinely consumed slightly more calories,
gained less weight, disposed of the extra calories as body heat 59 and vol-
untarily exercised more, 60 while still having far less cancer than animals
on standard diets. We found that calories were "burned" at a faster rate
and transformed into body heat as more oxygen was consumed. 59

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Understanding that diet can cause small shifts in calorie metabo-
lism that lead to big shifts in body weight is an important and useful
concept. It means that there is an orderly process of controlling body
weight over time that does work, as opposed to the disorderly process
of crash diets that don't work. It also accounts for the frequent observa-
tions (discussed in chapter six) that people who consume low-protein,
low-fat diets composed of whole plant foods have far less difficulty with
weight problems, even if they consume the same, or even slightly more,
total calories.

DIET AND BODY SIZE

We now know that eating a low-fat, low-protein diet high in complex
carbohydrates from fruits and vegetables will help you lose weight. But
what if you want to become bigger? A desire to be as big as possible
is pervasive in most cultures. During the colonial period in Asia and
Africa, Europeans even considered smaller people to be less civilized.
Body size seems to be a mark of prowess, manliness and dominance.

Most people think they can be bigger and stronger by eating protein-
rich animal-based foods. This belief stems from the idea that consuming
protein (a.k.a. meat) is needed for physical power. This has been a com-
mon notion the world over for a long time. The Chinese have even of-
ficially recommended a higher-protein diet in order to encourage bigger
athletes and to better compete in the Olympics. Animal-based foods have
more protein, and this protein is considered to be of "higher quality." Ani-
mal protein enjoys the same reputation in a rapidly modernizing China
as everywhere else.

There is, however, a problem with the idea that consuming animal-
based foods is a good way of becoming bigger. The people who eat the
most animal protein have the most heart disease, cancer and diabetes. In
the China Study, for example, animal protein consumption was associated
with taller and heavier 1 people, but was also associated with higher levels
of total and bad cholesterol." Furthermore, body weight, associated with
animal protein intake, 1 was associated with more cancer" " 1 and more cor-
onary heart disease." It seems that being bigger, and presumably better,
comes with very high costs. But might it be possible for us to achieve our
full growth potential, while simultaneously minimizing disease risks?

Childhood growth rates were not measured in the China Study but
adult height and weight were. This information proved surprising.
Consuming more protein was associated with greater body size ("' for

LESSONS FROM CHINA

103

men and " for women). 61 However, this effect was primarily attributed
to plant protein, because it makes up 90% of the total Chinese protein
intake. Animal protein consumption was indeed associated with greater
body weight, 1 and consumption of protein-rich milk seemed to be effec-
tive as well." But the good news is this: Greater plant protein intake was
closely linked to greater height" and body weight. 11 Body growth is linked
to protein in general and both animal and plant proteins are effective!

This means that individuals can achieve their genetic potential for
growth and body size by consuming a plant-based diet. So why is it that
people in developing nations, who consume little or no animal-based
foods, are consistently smaller than Western people? This is because
plant-based diets in poor areas of the world usually have insufficient
variety, inadequate quantity and quality and are associated with poor
public health conditions where childhood diseases are prevalent. Under
these conditions, growth is stunted and people do not reach their ge-
netic potential for adult body size. In the China Study low adult height
and weight were strongly associated with areas having high mortality
rates for pulmonary tuberculosis," 1 parasitic diseases, 1 " pneumonia ("'
for height), "intestinal obstruction" 1 " and digestive diseases. 1 "

These findings support the idea that body stature can be achieved
by consuming a low-fat, plant-based diet, provided that public health
conditions effectively control the diseases of poverty. Under these con-
ditions, the diseases of affluence (heart disease, cancers, diabetes, etc.)
can be simultaneously minimized.

The same low-animal protein, low-fat diet that helps prevent obesity
also allows people to reach their full growth potential while working
other wonders as well. It better regulates blood cholesterol and reduces
heart disease and a variety of cancers.

What are the odds that all of these associations (and many others)
favoring a plant-based diet are due to pure chance? It is extremely un-
likely, to say the least. Such consistency of evidence across a broad range
of associations is rare in scientific research. It points to a new worldview,
a new paradigm. It defies the status quo, promises new health benefits
and demands our attention.

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CIRCLING BACK

In the beginning of my career, I concentrated on the biochemical pro-
cesses of liver cancer. Chapter three delineates the decades-long labo-
ratory work we did with experimental animals, work that passed the
requirements to be called "good science." The finding: casein, and very
likely all animal proteins, may be the most relevant cancer-causing sub-
stances that we consume. Adjusting the amount of dietary casein has
the power to turn on and turn off cancer growth, and to override the
cancer-producing effects of afla toxin, a very potent Class IA carcinogen,
but even though these findings were substantially confirmed, they still
applied to experimental animals.

It was therefore with great anticipation that I looked to the China
Study for evidence on the causes of liver cancer in humans. 62

Liver cancer rates are very high in rural China, exceptionally high in
some areas. Why was this? The primary culprit seemed to be chronic
infection with hepatitis B virus (HBV). On average, about 12-13% of our
study subjects were chronically infected with the virus. In some areas,
one-half of the people were chronically infected! To put this into perspec-
tive, only 0.2-0.3% of Americans are chronically infected with this virus.

But there's more. In addition to the virus being a cause of liver cancer
in China, it seems that diet also plays a key role. How do we know? The
blood cholesterol levels provided the main clue. Liver cancer is strongly
associated with increasing blood cholesterol, 1 " and we already know
that animal-based foods are responsible for increases in cholesterol.

So, where does HBV fit in? The experimental mice studies gave a
good signal. In mice, HBV initiated the liver cancer but the cancer grew
in response to the feeding of higher levels of casein. In addition, blood
cholesterol also increased. These observations fit perfectly with our hu-
man findings. Individuals who are chronically infected with HBV and
who consume animal-based foods have high blood cholesterol and a
high rate of liver cancer. The virus provides the gun, and bad nutrition
pulls the trigger.

A very exciting story was taking shape, at least to my way of think-
ing. It was a story full of meaning and suggestive of important principles
that might apply to other diet and cancer associations. It also was a
story that had not been told to the public, and yet it was capable of sav-
ing lives. Eventually, it was a story that was leading to the idea that our
most powerful weapon against cancer is the food we eat every day.

LESSONS FROM CHINA

105

So there we had it. The years of animal experiments illuminated
profound biochemical principles and processes that greatly helped to
explain the effect of nutrition on liver cancer. But now we could see that
these processes were relevant for humans as well. People chronically
infected with hepatitis B virus also had an increased risk of liver cancer.
But our findings suggested those who were infected with the virus and
who were simultaneously eating more animal-based foods had higher
cholesterol levels and more liver cancer than those infected with the
virus and not consuming animal-based foods. The experimental animal
studies and the human studies made a perfect fit.

PULLING IT TOGETHER

Almost all of us in the United States will die of diseases of affluence. In
our China Study, we saw that nutrition has a very strong effect on these
diseases. Plant-based foods are linked to lower blood cholesterol; ani-
mal-based foods are linked to higher blood cholesterol. Animal-based
foods are linked to higher breast cancer rates; plant-based foods are
linked to lower rates. Fiber and antioxidants from plants are linked to a
lower risk of cancers of the digestive tract. Plant-based diets and active
lifestyles result in a healthy weight, yet permit people to become big and
strong. Our study was comprehensive in design and comprehensive in
its findings. From the labs of Virginia Tech and Cornell University to the
far reaches of China, it seemed that science was painting a clear, con-
sistent picture: we can minimize our risk of contracting deadly diseases
just by eating the right food.

When we first started this project we encountered significant resis-
tance from some people. One of my colleagues at Cornell, who had been
involved in the early planning of the China Study, got quite heated in
one of our meetings. I had put forth the idea of investigating how lots of
dietary factors, some known but many unknown, work together to cause
disease. Thus we had to measure lots of factors, regardless of whether or
not they were justified by prior research. If that was what we intended to
do, he said he wanted nothing to do with such a "shotgun" approach.

This colleague was expressing a view that was more in line with
mainstream scientific thought than with my idea. He and like-minded
colleagues think that science is best done when investigating single —
mostly known — factors in isolation. An array of largely unspecified fac-
tors doesn't show anything, they say. It's okay to measure the specific
effect of, say, selenium on breast cancer, but it's not okay to measure

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multiple nutritional conditions in the same study, in the hope of identi-
fying important dietary patterns.

I prefer the broader picture, for we are investigating the incredible
complexities and subtleties of nature itself. I wanted to investigate how
dietary patterns related to disease, now the most important point of this
book. Everything in food works together to create health or disease. The
more we think that a single chemical characterizes a whole food, the
more we stray into idiocy. As we shall see in Part IV of this book, this
way of thinking has generated a lot of poor science.

So I say we need more, not less, of the "shotgun approach." We need
more thought about overall dietary patterns and whole foods. Does this
mean that I think the shotgun approach is the only way to do research?
Of course not. Do I think that the China Study findings constitute abso-
lute scientific proof? Of course not. Does it provide enough information
to inform some practical decision-making? Absolutely.

An impressive and informative web of information was emerging
from this study. But does every potential strand (or association) in this
mammoth study fit perfectly into this web of information? No. Although
most statistically significant strands readily fit into the web, there were a
few surprises. Most, but not all, have since been explained.

Some associations observed in the China Study, at first glance, were
at odds with what might have been expected from Western experience.
I've had to use care in separating unusual findings that could be due
to chance and experimental insufficiency from those that truly offered
new insights into our old ways of thinking. As I mentioned earlier, the
range of blood cholesterol levels in rural China was a surprise. At the
time when the China Study was begun, a blood cholesterol range of
200-300 milligrams per deciliter (mg/dL) was considered normal, and
lower levels were suspect. In fact, some in the scientific and medical
communities considered cholesterol levels lower than 150 mg/dL to be
dangerous. In fact, my own cholesterol was 260 mg/dL in the late 1970s,
not unlike other members of my immediate family. The doctor told me
it was "fine, just average."

But when we measured the blood cholesterol levels in China, we
were shocked. They ranged from 70-170 mg/dL! Their high was our
low, and their low was off the chart you might find in your doctor's
office! It became obvious that our idea of "normal" values (or ranges)
only applies to Western subjects consuming the Western diet. It so
happens, for example, that our "normal" cholesterol levels present a

LESSONS FROM CHINA

107

significant risk for heart disease. Sadly, it's also "normal" to have heart
disease in America. Over the years, standards have been established that
are consistent with what we see in the West. We too often have come to
the view that U.S. values are "normal" because we have a tendency to
believe that the Western experience is likely to be right.

At the end of the day the strength and consistency of the majority
of the evidence is enough to draw valid conclusions. Namely, whole,
plant-based foods are beneficial, and animal-based foods are not. Few
other dietary choices, if any, can offer the incredible benefits of looking
good, growing tall and avoiding the vast majority or premature diseases
in our culture.

The China Study was an important milestone in my thinking. Standing
alone, it does not prove that diet causes disease. Absolute proof in science
is nearly unattainable. Instead, a theory is proposed and debated until the
weight of the evidence is so overwhelming that everyone commonly ac-
cepts that the theory is most likely true. In the case of diet and disease, the
China Study adds a lot of weight to the evidence. Its experimental features
(multiple diet, disease and lifestyle characteristics, and unusual range of
dietary experience, a good means of measuring data quality) provided an
unparalleled opportunity to expand our thinking about diet and disease
in ways that previously were not available. It was a study that was like a
flashlight that illuminated a path that I had never fully seen before.

The results of this study in addition to a mountain of supporting
research, some of it my own and some of it from other scientists, con-
vinced me to turn my dietary lifestyle around. I stopped eating meat
fifteen years ago, and I stopped eating almost all animal-based foods,
including dairy, within the past six to eight years, except on very rare
occasions. My cholesterol has dropped, even as I've aged; I am more
physically fit now than when I was twenty- five; and I am forty-five
pounds lighter now than I was when I was thirty years old. I am now at
an ideal weight for my height. My family has also adopted this way of
eating, thanks in large part to my wife Karen, who has managed to create
an entire new dietary lifestyle that is attractive, tasty and healthy. This
has all been done for health reasons, the result of my research findings
telling me to wake up. From a boyhood of drinking at least two quarts
of milk a day to an early professional career of scoffing at vegetarians, I
have taken an unusual turn in my life.

However, it has been more than my own research that has changed
my life. Over the years, I have gone well beyond our own research find-

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ings to see what other researchers have found regarding diet and health.
As our research findings expanded from the specific to the general, the
picture has continued to enlarge. We now can look at the work of other
scientists to put my findings into a larger context. As you shall see, it is
nothing short of astonishing.

Part II

DISEASES OF AFFLUENCE

Here in America, we are affluent, and we die certain deaths because of it.
We eat like feasting kings and queens every day of the week, and it kills
us. You probably know people who suffer from heart disease, cancer,
stroke, Alzheimer's, obesity or diabetes. There's a good chance that you
yourself suffer from one of these problems, or that one of these diseases
runs in your family. As we have seen, these diseases are relatively un-
known in traditional cultures that subsist mostly on whole plant foods,
as in rural China. But these ailments arrive when a traditional culture
starts accumulating wealth and starts eating more and more meat, dairy
and refined plant products (like crackers, cookies and soda).

In public lectures, 1 start my presentation by telling the audience
my personal story, just as 1 have done in this book. Invariably, I get a
question at the end of the lecture from someone who wants to know
more about diet and a specific disease of affluence. Chances are that you
yourself also have a question about a specific disease. Chances are, too,
that this specific disease is a disease of affluence, because that's what we
die of here in America.

You might be surprised to know that the disease that interests you
has much in common with other diseases of affluence, especially when
it comes to nutrition. There is no such thing as a special diet for cancer
and a different, equally special diet for heart disease. The evidence now
amassed from researchers around the world shows that the same diet
that is good for the prevention of cancer is also good for the prevention

109

110

THE CHINA STUDY

of heart disease, as well as obesity, diabetes, cataracts, macular degener-
ation, Alzheimer's, cognitive dysfunction, multiple sclerosis, osteoporo-
sis and other diseases. Furthermore, this diet can only benefit everyone,
regardless of his or her genes or personal dispositions.

All of these diseases, and others, spring forth from the same influ-
ence: an unhealthy, largely toxic diet and lifestyle that has an excess of
sickness-promoting factors and a deficiency of health-promoting fac-
tors. In other words, the Western diet. Conversely, there is one diet to
counteract all of these diseases: a whole foods, plant-based diet.

The following chapters are organized by disease, or disease grouping.
Each chapter contains evidence showing how food relates to each dis-
ease. As you go through each chapter, you will begin to see the breadth
and depth of the astonishing scientific argument favoring a whole foods,
plant-based diet. For me, the consistency of evidence regarding such a
disparate group of diseases has been the most convincing aspect of this
argument. When a whole foods, plant-based diet is demonstrably ben-
eficial for such a wide variety of diseases, is it possible that humans were
meant to consume any other diet? I say no, and I think you'll agree.

America and most other Western nations have gotten it wrong when
it comes to diet and health, and we have paid a grave price. We are sick,
overweight and confused. As I have moved on from the laboratory stud-
ies and the China Study and encountered the information discussed in
Part II, I have become overwhelmed. I have come to realize that some
of our most revered conventions are wrong and real health has been
grossly obscured. Most unfortunately, the unsuspecting public has paid
the ultimate price. In large measure, this book is my effort to right these
wrongs. As you will come to see in the following chapters, from heart
disease to cancer, and from obesity to blindness, there is a better path
to optimal health.

Broken Hearts

Put your hand on your chest and feel your heart beat. Now put your
hand where you can feel your pulse. That pulse is the signature of your
being. Your heart, creating that pulse, is working for you every minute
of the day every day of the year, and every year of your entire life. If you
live an average lifetime, your heart will beat about 3 billion times. 1

Now take a moment to realize that during the time it took you to
read the above paragraph an artery in the heart of roughly one American
clogged up, cut off blood flow and started a rapid process of tissue and
cell death. This process is better known, of course, as a heart attack. By
the time you finish reading this page, four Americans will have had a
heart attack, and another four will have fallen prey to stroke or heart
failure. 2 Over the next twenty-four hours, 3,000 Americans will have
heart attacks, 2 roughly the same number of people who perished in the
terrorist attacks of September 11, 2001.

The heart is the centerpiece of life and, more often than not in Ameri-
ca, it is the centerpiece of death. Malfunction of the heart and/or circula-
tion system will kill 40% of Americans, 3 more than those killed by any
other injury or ailment, including cancer. Heart disease has been our
number one cause of death for almost one hundred years. 4 This disease
does not recognize gender or race boundaries; all are affected. If you
were to ask most women what disease poses the greatest risk to them,
heart disease or breast cancer, many women would undoubtedly say
breast cancer. But they would be wrong. Women's death rate from heart
disease is eight times higher than their death rate from breast cancer. 5 6

Ill

112

THE CHINA STUDY

If there is an "American" game, it is baseball; an "American" dessert,
apple pie. If there is an "American" disease, it is heart disease.

EVERYONE'S DOING IT

In 1950, Judy Holliday could be seen on the big screen, Ben Hogan
dominated the world of golf, the musical South Pacific won big at the
Tony Awards and on June 25, North Korea invaded South Korea. The
American administration was taken aback but responded quickly. With-
in days, President Truman sent in troops on the ground and bombers
overhead to push back the North Korean army. Three years later, in July
of 1953, a formal cease-fire agreement had been signed and the Korean
War was over. During this period of time, over 30,000 American sol-
diers were killed in battle.

At the end of the war, a landmark scientific study was reported in the
Journal of the American Medical Association. Military medical investiga-
tors had examined the hearts of 300 male soldiers killed in action in Ko-
rea. The soldiers, at an average age of twenty-two years, had never been
diagnosed with heart problems. In dissecting these hearts, researchers
found startling evidence of disease in an exceptional number of cases.
Fully 77.3% of the hearts they examined had "gross evidence" of heart dis-
ease. 7 (In this instance, "gross" means large.)

That number, 77.3%, is startling. Coming at a time when our number
one killer was still shrouded in mystery, the research clearly demon-
strated that heart disease develops over an entire lifetime. Furthermore,
almost everyone was susceptible! These soldiers were not couch-potato
slouches; they were in top condition in the prime of their physical lives.
Since that time, several other studies have confirmed that heart disease
is pervasive in young Americans. 8

THE HEART ATTACK

But what is heart disease? One of the key components is plaque. Plaque
is a greasy layer of proteins, fats (including cholesterol), immune sys-
tem cells and other components that accumulate on the inner walls of
the coronary arteries. I have heard one surgeon say that if you wipe
your finger on a plaque-covered artery, it has the same feel as wiping
your finger across a warm cheesecake. If you have plaque building up
in your coronary arteries, you have some degree of heart disease. Of
the autopsied soldiers in Korea, one out of twenty diseased men had so
much plaque that 90% of an artery was blocked. 7 That's like putting a

BROKEN HEARTS

113

kink in a garden hose and watering a desperately dry garden with the
resulting trickle of water!

Why hadn't these soldiers had a heart attack already? After all, only
10% of the artery was open. How could that be enough? It turns out
that if the plaque on the inner wall of the artery accumulates slowly,
over several years, blood flow has time to adjust. Think of blood flowing
through your artery as a raging river. If you put a few stones on the sides
of a river every day over a period of years, like plaque accumulating on
the walls of the artery, the water will find another way to get to where it
wants to be. Maybe the river will form several smaller streams over the
stones. Perhaps the river will go under the stones forming tiny tunnels,
or maybe the water will flow through small side streams, taking a new
route altogether. These new tiny passageways around or through the
stones are called "collaterals." The same thing happens in the heart. If
plaque accumulates over a period of several years there will be enough
collateral development that blood can still travel throughout the heart.
However, too much plaque buildup can cause severe blood restriction,
and debilitating chest pain, or angina, can result. But this buildup only
rarely leads to heart attacks. 9, 10

So what leads to heart attacks? It turns out that it's the less severe ac-
cumulations of plaque, blocking under 50% of the artery, that often cause
heart attacks. 11 These accumulations each have a layer of cells, called the
cap, which separates the core of the plaque from the blood flowing by. In
the dangerous plaques, the cap is weak and thin. Consequently, as blood
rushes by, it can erode the cap until it ruptures. When the cap ruptures,
the core contents of the plaque mix with the blood. The blood then begins
clotting around the site of rupture. The clot grows and can quickly block
off the entire artery. When the artery becomes blocked over such a short
period of time, there is litde chance for collateral blood flow to develop.
When this happens, blood flow downstream of the rupture is severely
reduced and the heart muscles don't get the oxygen they require. At this
point, as heart muscle cells start to die, heart pumping mechanisms begin
to fail, and the person may feel a crushing pain in the chest, or a searing
pain down into an arm and up into the neck and jaw. In short, the victim
starts to die. This is the process behind most of the 1 . 1 million heart at-
tacks that occur in America every year. One out of three people who have
a heart attack will die from it. 9, 10

We now know that the small to medium accumulation of plaque, the
plaque that blocks less than 50% of the artery, is the most deadly. 11 ' 12

THE CHINA STUDY

So how can we predict the timing of heart attacks? Unfortunately, with
existing technologies, we can't. We can't know which plaque will rup-
ture, when, or how severe it might be. What we do know, however, is
our relative risk for having a heart attack. What once was a mysterious
death, which claimed people in their most productive years, has been
"demystified" by science. No study has been more influential than that
of the Framingham Heart Study.

FRAMINGHAM

After World War II, the National Heart Institute 13 was created with a
modest budget 4 and a difficult mission. Scientists knew that the greasy
plaques that lined the arteries of diseased hearts were composed of cho-
lesterol, phospholipids and fatty acids, 14 but they didn't know why these
lesions developed, how they developed or exactly how they led to heart
attacks. In the search for answers, the National Heart Institute decided
to follow a population over several years, to keep detailed medical re-
cords of everybody in the population and to see who got heart disease
and who didn't. The scientists headed to Framingham, Massachusetts.

Located just outside of Boston, Framingham is steeped in American
history. European settlers first inhabited the land in the seventeenth
century. Over the years the town has had supporting roles in the Revo-
lutionary War, the Salem Witch Trials and the abolition movement.
More recently, in 1948, the town assumed its most famous role. Over
5,000 residents of Framingham, both male and female, agreed to be
poked and prodded by scientists over the years so that we might learn
something about heart disease.

And learn something we did. By watching who got heart disease
and who didn't, and comparing their medical records, the Framingham
Heart Study developed the concept of risk factors such as cholesterol,
blood pressure, physical activity, cigarette smoking and obesity. Because
of the Framingham Study, we now know that these risk factors play a
prominent role in the causation of heart disease. Doctors have for years
used a Framingham prediction model to tell who is at high risk for heart
disease and who is not. Over 1,000 scientific papers have been pub-
lished from this study, and the study continues to this day, having now
studied four generations of Framingham residents.

The shining jewel of the Framingham Study is its findings on blood
cholesterol. In 1961, they convincingly showed a strong correlation be-
tween high blood cholesterol and heart disease. Researchers noted that

BROKEN HEARTS

115

men with cholesterol levels "over 244 mg/dL (milligrams per deciliter)
have more than three times the incidence of CHD (coronary heart dis-
ease) as do those with cholesterol levels less than 210 mg/dL." 15 The
contentious question of whether blood cholesterol levels could predict
heart disease was laid to rest. Cholesterol levels do make a difference.
In this same paper, high blood pressure was also demonstrated to be an
important risk factor for heart disease.

The importance given to risk factors signaled a conceptual revolu-
tion. When this study was started, most doctors believed that heart
disease was an inevitable "wearing down" of the body, and we could do
little about it. Our hearts were like car engines; as we got older, the parts
didn't work as well and sometimes gave out. By demonstrating that we
could see the disease in advance by measuring risk factors, the idea of
preventing heart disease suddenly had validity. Researchers wrote, "... it
appears that a preventive program is clearly necessary." 15 Simply lower
the risk factors, such as blood cholesterol and blood pressure, and you
lower the risk of heart disease.

In modern-day America cholesterol and blood pressure are house-
hold terms. We spend over 30 billion dollars a year on drugs to control
these risk factors and other aspects of cardiovascular disease. 2 Almost
everyone now knows that he or she can work to prevent a heart attack
by keeping his or her risk factors at the right levels. This awareness is
only about fifty years old and due in large measure to the scientists and
subjects of the Framingham Heart Study.

OUTSIDE OUR BORDERS

Framingham is the most well-known heart study ever done, but it is
merely one part of an enormous body of research conducted in this
country over the past sixty years. Early research led to the alarming
conclusion that we have some of the highest rates of heart disease in
the world. One study published in 1959 compared the coronary heart
disease death rates in twenty different countries (Chart 5.1). 16

These studies were examining Westernized societies. If we look at
more traditional societies, we tend to see even more striking disparities
in the incidence of heart disease. The Papua New Guinea Highlanders,
for example, pop up in research quite a bit because heart disease is rare
in their society. 17 Remember, for example, how low the rate of heart dis-
ease was in rural China. American men died from heart disease at a rate
almost seventeen times higher than their Chinese counterparts. 18

116

THE CHINA STUDY

CHART 5.1: HEART DISEASE DEATH RATES FOR MEN AGED 55 TO 59
ACROSS 20 COUNTRIES, CIRCA 1955 16

800'/

700

o
o
o

o"
o

600

500

40C

300

CD
Q

200

100

Why were we succumbing to heart disease in the sixties and seven-
ties, when much of the world was relatively unaffected?

Quite simply it was a case of death by food. The cultures that have
lower heart disease rates eat less saturated fat and animal protein and
more whole grains, fruits and vegetables. In other words, they subsist
mostly on plant foods while we subsist mostly on animal foods.

But might it be that the genetics of one group might just make them
more susceptible to heart disease? We know that this is not the case,
because within a group with the same genetic heritage, a similar rela-
tionship between diet and disease is seen. For example, Japanese men
who live in Hawaii or California have a much higher blood cholesterol
level and incidence of coronary heart disease than Japanese men living
in Japan. 19 ' 20

The cause is clearly environmental, as most of these people have the
same genetic heritage. Smoking habits are not the cause because men

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117

in Japan, who were more likely to smoke, still had less coronary heart
disease than the Japanese Americans. 19 The researchers pointed to diet,
writing that blood cholesterol increased "with dietary intake of satu-
rated fat, animal protein and dietary cholesterol." On the flip side, blood
cholesterol "was negatively associated with complex carbohydrate in-
take " 20 In simple terms, animal foods were linked to higher blood

cholesterol; plant foods were linked to lower blood cholesterol.

This research clearly implicated diet as one possible cause of heart
disease. Furthermore, the early results were painting a consistent pic-
ture: the more saturated fat and cholesterol (as indicators of animal food
consumption) people eat, the higher their risk for getting heart disease.
And as other cultures have come to eat more like us, they also have
seen their rates of heart disease skyrocket. In more recent times, several
countries have now come to have a higher death rate from heart disease
than America.

RESEARCH AHEAD OF ITS TIME

So now we know what heart disease is and what factors determine our
risk for it, but what do we do once the disease is upon us? When the
Framingham Heart Study was just beginning, there were already doc-
tors who were trying to figure out how to treat heart disease, rather
than just prevent it. In many ways, these investigators were ahead of
their time because their interventions, which were the most innovative,
successful treatment programs at the time, utilized the least advanced
technology available: the knife and fork.

These doctors noticed the ongoing research at the time and made
some common-sense connections. They realized that 21 :

• excess fat and cholesterol consumption caused atherosclerosis (the
hardening of the arteries and the accumulation of plaque) in ex-
perimental animals

• eating cholesterol in food caused a rise in cholesterol in the blood

• high blood cholesterol might predict and/or cause heart disease

• most of the world's population didn't have heart disease, and these
heart disease-free cultures had radically different dietary patterns,
consuming less fat and cholesterol

So they decided to try to alter heart disease in their patients by having
them eat less fat and cholesterol.

One of the most progressive doctors was Dr. Lester Morrison of Los

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Angeles. He started a study in 1946 (two years before the Framingham
Study) to "determine the relationship of dietary fat intake to the inci-
dence of atherosclerosis." 22 In his study he instructed fifty heart attack
survivors to maintain their normal diet and fifty different heart attack
survivors to consume an experimental diet.

In the experimental diet group he reduced the consumption of fat and
cholesterol. One of his published sample menus allowed the patient to
have only a small amount of meat two times a day: two ounces of "cold
roast lamb, lean, with mint jelly" for lunch, and another two ounces of
"lean meats" for dinner. 22 Even if you loved cold roast lamb with mint
jelly, you weren't allowed to eat much of it. In fact, the list of prohibited
foods in the experimental diet was fairly long and included cream soups,
pork, fat meats, animal fats, whole milk, cream, butter, egg yolks and
breads and desserts made with butter, whole eggs and whole milk. 22

Did this progressive diet accomplish anything? After eight years,
only twelve of fifty people eating their normal American diet were alive
(24%). In the diet group, twenty-eight people were still alive (56%),
almost two and one-half times the amount of survivors in the control
group. After twelve years, every single patient in the control group was
dead. In the diet group, however, nineteen people were still alive, a
survival rate of 38%. 22 While it was unfortunate that so many people in
the dietary group still died, it was clear that they were staving off their
disease by eating moderately less animal foods and moderately more
plant foods (see Chart 5.2).

CHART 5.2: SURVIVAL RATE OF DR. MORRISON'S PATIENTS

0 3 8 12

Time (years)

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119

In 1946, when this study began, most scientists believed that heart
disease was an inevitable part of aging, and nothing much could be done
about it. While Morrison didn't cure heart disease, he proved that some-
thing as simple as diet could significantly alter its course, even when the
disease is so advanced that it has already caused a heart attack.

Another research group proved much the same thing at about that
time. A group of doctors in Northern California took a larger group of
patients with advanced heart disease and put them on a low-fat, low-
cholesterol diet. These doctors found that the patients who ate the low-
fat, low-cholesterol diet died at a rate four times lower than patients who
didn't follow the diet. 23

It was now clear that there was hope. Heart disease wasn't the inevi-
table result of old age, and even when a person had advanced disease, a
low-fat, low-cholesterol diet could significantly prolong his or her life.
This was a remarkable advance in our understanding of the number one
killer in America. Furthermore, this new understanding made diet and
other environmental factors the centerpieces of heart disease. Any dis-
cussion of diet, however, was narrowly focused on fat and cholesterol.
These two isolated food components became the bad guys.

We now know that the attention paid to fat and cholesterol was mis-
guided. The possibility that no one wanted to consider was that fat and
cholesterol were merely indicators of animal food intake. For example,
look at the relationship between animal protein consumption and heart
disease death in men aged fifty-five to fifty-nine across twenty different
countries in Chart 5. 3. 16

This study suggests that the more animal protein you eat, the more
heart disease you have. In addition, dozens of experimental studies
show that feeding rats, rabbits and pigs animal protein (e.g., casein)
dramatically raises cholesterol levels, whereas plant protein (e.g., soy
protein) dramatically lowers cholesterol levels. 24 Studies in humans not
only mirror these findings, but show that eating plant protein has even
greater power to lower cholesterol levels than reducing fat or choles-
terol intake. 25

While some of these studies implicating animal protein were con-
ducted in the past thirty years, others were published well over fifty
years ago when the health world was first beginning to discuss diet and
heart disease. Yet somehow animal protein has remained in the shadows
while saturated fat and cholesterol have taken the brunt of the criticism.
These three nutrients (fat, animal protein and cholesterol) characterize

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CHART 5.3: HEART DISEASE DEATH RATES FOR MEN
AGED 55 TO 59 YEARS AND ANIMAL PROTEIN CONSUMPTION
ACROSS 20 COUNTRIES' 6

Percent of total calories coming from animal protein

animal-based food in general. So isn't it perfectly reasonable to wonder
whether animal-based food, and not just these isolated nutrients, causes
heart disease?

Of course, no one pointed a finger at animal-based foods in general.
It would have led immediately to professional isolation and ridicule
(for reasons discussed in Part IV). These were contentious times in
the nutritional world. A conceptual revolution was taking place, and
a lot of people didn't like it. Even talking about diet was too much for
many scientists. Preventing heart disease by diet was a threatening idea
because it implied that something about the good old meaty American
diet was so bad for us that it was destroying our hearts. The status quo
boys didn't like it.

One status quo scientist had a good time making fun of people who
appeared to have a low risk of heart disease. In 1960, he wrote the fol-
lowing piece of "humor" to mock the then-recent findings 26 :

Thumbnail Sketch of the Man Least Likely
to Have Coronary Heart Disease:

An effeminate municipal worker or embalmer, completely lacking
in physical and mental alertness and without drive, ambition or
competitive spirit who has never attempted to meet a deadline of
any kind. A man with poor appetite, subsisting on fruit and veg-
etables laced with corn and whale oils, detesting tobacco, spurning

BROKEN HEARTS

121

ownership of radio, TV or motor car, with full head of hair and
scrawny and un-athletic in appearance, yet constantly straining
his puny muscles by exercise; low in income, B.P. (blood pressure),
blood sugar, uric acid and cholesterol, who has been taking nico-
tinic acid, pyridoxine and long term anticoagulant therapy ever
since his prophylactic castration.

The author of this passage might just as well have said, "Only REAL
men have heart disease." Also notice how a diet of fruits and vegetables
is described as "poor" even though the author suggests that this diet
is eaten by those people who are least likely to have heart disease. The
unfortunate association of meat with physical ability, general manliness,
sexual identity and economic wealth all cloud how the status quo scien-
tists viewed food, regardless of the health evidence. This view had been
passed down from the early protein pioneers described in chapter two.

Perhaps this author should have met a friend of mine, Chris Camp-
bell (no relation). Chris is a two-time NCAA Division 1 wrestling cham-
pion, three-time U.S. Senior wrestling champion, two-time Olympic
wrestler and Cornell Law School graduate. At the age of thirty-seven
he became the oldest American ever to win an Olympic medal in wres-
tling, weighing in at 198 pounds. Chris Campbell is a vegetarian. As a
man not likely to have heart disease, 1 think he might disagree with the
characterization above.

The battle between the status quo and the dietary prevention camp
was intense. I remember attending a lecture at Cornell University dur-
ing the late 1950s when a famous researcher, Ancel Keys, came to talk
about preventing heart disease by diet. Some scientists in the audience
just shook their heads in disbelief, saying diet can't possibly affect heart
disease. In those first decades of heart disease research, a heated, per-
sonal battle flared, and open-mindedness was the first casualty.

RECENT HISTORY

Today, this epic battle between defenders of the status quo and advo-
cates of diet is as strong as ever. But there have been significant changes
in the landscape of heart disease. How far have we come, and how have
we proceeded to fight this disease? Mostly the status quo has been pro-
tected. Despite the potential of diet and disease prevention, most of the
attention given to heart disease has been on mechanical and chemical
intervention for those people who have advanced disease. Diet has been

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pushed aside. Surgery, drugs, electronic devices and new diagnostic
tools have stolen the spotlight.

We now have coronary bypass surgery, where a healthy artery is
"pasted" over a diseased artery, thereby bypassing the most dangerous
plaque on the artery. The ultimate surgery, of course, is the heart trans-
plant, which even utilizes an artificial heart on occasion. We also have
a procedure that doesn't require cracking the chest plate open, called
coronary angioplasty, where a small balloon is inflated in a narrowed,
diseased artery, squishing the plaque back against the wall, opening up
the passage for increased blood flow. We have defibrillators to revive
hearts, pacemakers and precise imaging techniques so that we can ob-
serve individual arteries without having to expose the heart.

The past fifty years have truly been a celebration of chemicals and
technology (as opposed to diet and prevention). In summarizing the
initial widespread research on heart disease, one doctor recently high-
lighted the mechanical:

It was hoped that the strength of science and engineering devel-
oped after World War II could be applied to this battle [against
heart disease] The enormous advances in mechanical engineer-
ing and electronics that had been stimulated by the war seemed to
lend themselves particularly well to the study of the cardiovascu-
lar system 4

Some great advances have been made, to be sure, which may account
for the fact that our death rate from heart disease is a full 58% lower
than what it was in 1950. 2 A 58% reduction in the death rate seems a
great victory for chemicals and technology. One of the greatest strides
has come from better emergency room treatment of heart attack vic-
tims. In 1970, if you were older than sixty-five years, had a heart attack
and were lucky enough to make it to the hospital alive, you had a 38%
chance of dying. Today, if you make it to the hospital alive, you only
have a 15% chance of dying. The hospital's emergency response is much
better, and consequently huge numbers of lives are being spared. 2

In addition, the number of people smoking has steadily been decreas-
ing, 2728 which in turn lowers our death rate from heart disease. Between
hospital advances, mechanical devices, drug discoveries, lower smoking
rates and more surgical options, there clearly seems to be much to cheer
about. We've made progress, so it seems.

Or have we?

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123

After all, heart disease is still our number one cause of death. Every
twenty-four hours, almost 2,000 Americans will die from this disease. 2
For all the advances, there are a huge number of people still succumb-
ing to broken hearts.

In fact, the incidence rate (not death rate) for heart disease 29 is about
the same as it was in the early 1970s. 2 In other words, while we don't
die as much from heart disease, we still get it as often as we used to. In
seems that we simply have gotten slightly better at postponing death
from heart disease, but we have done nothing to stop the rate at which our
hearts become diseased,

SURGERY: THE PHANTOM SAVIOR

The mechanical interventions that we use in this country are much less
effective than most people realize. Bypass surgery has become particu-
larly popular. As many as 380,000 bypass operations were performed
in 1990, 30 meaning that about 1 out of 750 Americans underwent this
extreme surgery. During the operation, the patient's chest is split open,
blood flow is rerouted by a series of clamps, pumps and machines, and
a leg vein or chest artery is cut out and sewn over a diseased part of the
heart, thereby allowing blood to bypass the most clogged arteries.

The costs are enormous. More than one of every fifty elective patients
will die because of complications 31 during the $46,000 procedure. 32
Other side effects include heart attack, respiratory complications, bleed-
ing complications, infection, high blood pressure and stroke. When the
vessels around the heart are clamped shut during the operation, plaque
breaks off of the inner walls. Blood then carries this debris to the brain,
where it causes numerous "mini" strokes. Researchers have compared
the intellectual capabilities of patients before and after the operation,
and found that a stunning 79% of patients "showed impairment in some
aspect of cognitive function" seven days after the operation. 33

Why do we put ourselves through this? The most pronounced ben-
efit of this procedure is relief of angina, or chest pain. About 70-80% of
patients who undergo bypass surgery remain free of this crippling chest
pain for one year. 34 But this benefit doesn't last. Within three years of the
operation, up to one-third of patients will suffer from chest pain again. 35
Within ten years half of the bypass patients will have died, had a heart
attack or had their chest pain return. 36 Long-term studies indicate that
only certain subsets of heart disease patients live longer because of their
bypass operation. 12 Furthermore, these studies demonstrate that those

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patients who undergo bypass operation do not have fewer heart attacks than
those who do not have surgery. 12

Remember which plaque buildups cause heart attacks? The deadly
buildups are the smaller, less stable plaques that tend to rupture. The by-
pass operation, however, is targeted to the largest, most visible plaques,
which may be responsible for chest pain, but not for heart attacks.

Angioplasty is a similar story. The procedure is expensive and carries
significant risks. After identifying blockages in a coronary artery, a bal-
loon is inserted into the artery and inflated. It pushes the plaque back
against the vessel, thereby allowing more blood to flow. Roughly one
out of sixteen patients will experience an "abrupt vessel closure" during
the procedure, which can lead to death, heart attack or an emergency
bypass operation. 37 Assuming that doesn't happen, there is still a good
chance that the procedure will fail. Within four months after the proce-
dure, 40% of the arteries that were "squished" open will close up again,
effectively nullifying the procedure. 38 Nonetheless, barring these unfa-
vorable outcomes, angioplasty does a good job of providing temporary
relief of chest pain. Of course, angioplasty does little to treat the small
blockages that are most likely to lead to heart attacks.

So, upon closer examination, our seemingly beneficent mechanical
advances in the field of heart disease are severely disappointing. Bypass
surgery and angioplasty do not address the cause of heart disease, prevent
heart attacks or extend the lives of any but the sickest heart disease pa-
tients.

What's going on here? Despite the positive public relations surround-
ing the past fifty years of heart disease research, we must ask ourselves:
are we winning this war? Maybe we should ask ourselves what we might
do differently. For example, whatever happened to the dietary lessons
learned fifty years ago? Whatever happened to the dietary treatments
discovered by Dr. Lester Morrison, as discussed earlier?

Those discoveries largely faded away. I only learned about this
1940s and 1950s research in recent years. I am bewildered because
the professionals I heard during my graduate student days in the late
1950s and early 1960s vigorously denied that any such work was be-
ing done or even being contemplated. In the meanwhile, America's
eating habits have only gotten worse. According to the U.S. Depart-
ment of Agriculture, we consume significantly more meat and added
fat than we did thirty years ago. 39 Clearly we are not moving in the
right direction.

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125

As this information has resurfaced in the past two decades, the fight
against the status quo has been heating up again. A few rare doctors are
proving that there is a better way to defeat heart disease. They are dem-
onstrating revolutionary success, using the most simple of all treatments:
food.

DR. CALDWELL B. ESSELSTYN, JR.

If you were to guess the location of the best cardiac care center in the
country, maybe the world, what city would you name? New York? Los
Angeles? Chicago? A city in Florida, perhaps, near elderly people? As
it turns out, the best medical center for cardiac care is located in Cleve-
land, Ohio, according to US News and World Report. Patients fly in to the
Cleveland Clinic from all over the world for the most advanced heart
treatment available, administered by prestigious doctors.

One of the doctors at the Clinic, Dr. Caldwell B. Esselstyn, Jr. has
quite a resume. As a student at Yale University, Dr. Esselstyn rowed in
the 1956 Olympics, winning a gold medal. After being trained at the
Cleveland Clinic, he went on to earn the Bronze Star as an army surgeon
in the Vietnam War. He then became a highly successful doctor at one
of the top medical institutions in the world, the Cleveland Clinic, where
he was president of the staff, member of the Board of Governors, chair-
man of the Breast Cancer Task Force and head of the Section of Thyroid
and Parathyroid Surgery. Having published over 100 scientific papers,
Dr. Esselstyn was named one of the best doctors in America in 1994-
1995. 40 From knowing this man personally, I get the feeling that he has
excelled at virtually everything he has done in his life. He reached the
pinnacle of success in his professional and personal life, and did it with
grace and humility.

The quality I find most appealing about Dr. Esselstyn, however, is not
his resume or awards; it is his principled search for the truth. Dr. Essel-
styn has had the courage to take on the establishment. For the Second
National Conference on Lipids in the Elimination and Prevention of
Coronary Artery Disease (which he organized and in which he kindly
asked me to participate) Dr. Esselstyn wrote:

Eleven years into my career as a surgeon, I became disillusioned
with the treatment paradigm of U.S. medicine in cancer and heart
disease. Little had changed in 100 years in the management of
cancer, and in neither heart disease nor cancer was there a serious

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effort at prevention. I found the epidemiology of these diseases
provocative, however: Three-quarters of the humans on this plan-
et had no heart disease, a fact strongly associated with diet. 41

Dr. Esselstyn started to reexamine the standard medical practice.
"Aware that medical, angiographic and surgical interventions were
treating only the symptoms of heart disease and believing that a funda-
mentally different approach to treatment was necessary," Dr. Esselstyn
decided to test the effects of a whole foods, plant-based diet on people
with established coronary disease. 42 By using a minimal amount of cho-
lesterol-lowering medication and a very low-fat, plant-based diet, he
has gotten the most spectacular results ever recorded in the treatment
of heart disease. 42 43

In 1985, Dr. Esselstyn began his study with the primary goal of re-
ducing his patients' blood cholesterol to below 150 mg/dL. He asked
each patient to record everything he or she ate in a food diary. Every
two weeks, for the next five years, Dr. Esselstyn met with his patients
to discuss the process, administer blood tests and record blood pres-
sure and weight. He followed up this daytime meeting with an evening
telephone call to report the results of the blood tests and further discuss
how the diet was working. In addition, all of his patients met together
a few times a year to talk about the program, socialize and exchange
helpful information. In other words, Dr. Esselstyn was diligent, in-
volved, supportive and compassionately stern on a personal level with
his patients.

The diet they, including Dr. Esselstyn and his wife Ann, followed was
free of all added fat and almost all animal products. Dr. Esselstyn and
his colleagues report, "[Participants] were to avoid oils, meat, fish, fowl
and dairy products, except for skim milk and nonfat yogurt." 42 About
five years into the program, Dr. Esselstyn recommended to his patients
that they stop consuming any skim milk and yogurt, as well.

Five of his patients dropped out of the study within the first two
years; that left eighteen. These eighteen patients originally had come
to Dr. Esselstyn with severe disease. Within the eight years leading up to
the study, these eighteen people had suffered through forty-nine coronary
events, including angina, bypass surgery, heart attacks, strokes and an-
gioplasty. These were not healthy hearts. One might imagine that they
were motivated to join the study by the panic created when premature
death is near. 42,43

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127

These eighteen patients achieved remarkable success. At the start of
the study, the patients' average cholesterol level was 246 mg/dL. During
the course of the study, the average cholesterol was 132 mg/dL, well below
the 150 mg/dL target!'* 3 Their levels of "bad" LDL cholesterol dropped
just as dramatically. 42 In the end, though, the most impressive result
was not the blood cholesterol levels, but how many coronary events oc-
curred since the start of the study.

In the following eleven years, there was exactly ONE coronary event
among the eighteen patients who followed the diet. That one event was
from a patient who strayed from the diet for two years. After straying,
the patient consequently experienced clinical chest pain (angina) and
then resumed a healthy plant-based diet. The patient eliminated his an-
gina, and has not experienced any further events. 43

Not only has the disease in these patients been stopped, it has even
been reversed. Seventy percent of his patients have seen an opening of their
clogged arteries. 43 Eleven of his patients had agreed to angiography, a
procedure in which specific arteries in the heart can be "x-rayed." Of
these eleven, the blockages in the arteries were, on average, reduced in
size by 7% over the first five years of his study. This may sound like a
small change but it should be noted that the volume of blood delivered
is at least 30% greater when the diameter is increased by 7%. 44 More
importantly this is the difference between the presence of pain (from
angina) and absence of pain, indeed between life and death. Authors of
the five-year report note, "This is the longest study of minimal fat nutri-
tion used in combination with cholesterol-lowering drugs conducted to
date, and our finding of a mean decrease of arterial stenosis [blockage]
of 7.0% is greater than any reports in previous research." 42

One physician took special note of Dr. Esselstyn's study. He was only
forty-four years of age and seemingly healthy when he found himself
with a heart problem, culminating in a heart attack. Because of the na-
ture of his heart disease, there was nothing that conventional medicine
could safely offer him. He visited Dr. Esselstyn, decided to commit to
the dietary program, and after thirty-two months, without any choles-
terol-lowering medication, he reversed his heart disease and lowered his
blood cholesterol to 89 mg/dL. What follows is the dramatic image of this
patient's diseased artery before and after Dr. Esselstyn's dietary advice
(Chart 5.4). 8 The light part of the picture is blood flowing through an
artery. The picture on the left (A) has a section marked by a parenthesis
where severe coronary disease reduced the amount of blood flow. After

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CHART 5.4: CORONARY ARTERY BEFORE AND AFTER
CONSUMING PLANT-BASED DIET

adopting a whole foods, plant-based diet, that same artery opened up,
reversing the ravages of heart disease and allowing a much more normal
blood flow, as shown in the picture on the right (B).

Is it possible that Dr. Esselstyn just got a lucky group of patients? The
answer is no. Patients this sick with heart disease don't spontaneously
heal themselves. Another way to check the likelihood of this degree of
success is to look at the five patients that dropped out of the dietary pro-
gram and resumed their standard care. As of 1995, these five people had
fallen prey to ten new coronary events. 41 Meanwhile, as of 2003, seventeen
years into the study, all but one patient following the diet are still alive,
headed into their seventies and eighties. 43

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129

Can any sane person dispute these findings? It seems impossible. If
you remember nothing else about this chapter, remember the forty-nine
to zero score; forty-nine coronary events prior to a whole foods, plant-
based diet, and zero events for those patients who adhered to a whole
foods, plant-based diet. Dr. Esselstyn has done what "Big Science" has
been trying to do, without success, for over fifty-five years: he defeated
heart disease.

DR. DEAN ORNISH

In the past fifteen years another giant in this field, Dr. Dean Ornish, has
been instrumental in bringing diet to the forefront of medical thought.
A graduate of Harvard Medical School, he has been featured prominent-
ly in popular media, succeeded in having his heart disease treatment
plan covered by a number of insurance carriers and written several best-
selling books. If you have heard of the diet/heart disease connection,
chances are that it may well be because of Dr. Ornish's work.

His best-known research is the Lifestyle Heart Trial, in which he
treated twenty-eight heart disease patients with lifestyle changes
alone. 46 He put these patients on an experimental treatment plan and
twenty additional patients on the standard treatment plan. He followed
both groups carefully and measured several health indicators, including
artery blockages, cholesterol levels and weight.

Dr. Ornish's treatment plan was very different from the standards of
high-tech modern medicine. He put the twenty-eight patients in a hotel
for the first week of treatment and told them what they had to do to take
control of their health. He asked them to eat a low-fat, plant-based diet
for at least a year. Only about 10% of their calories were to come from
fat. They could eat as much food as they wanted, as long as it was on
the acceptable food list, which included fruits, vegetables and grains. As
researchers noted, "No animal products were allowed except egg white
and one cup per day of non-fat milk or yogurt." 46 In addition to diet, the
group was to practice various forms of stress management, including
meditation, breathing exercises and relaxation exercises for at least one
hour per day. The patients were also asked to exercise three hours per
week at levels customized to the severity of their disease. To help the pa-
tients make these lifestyle changes, the group met twice a week for four
hours at a time for mutual support. Dr. Ornish and his research group
did not use any drugs, surgery or technology to treat these patients. 46

The experimental patients adhered to pretty much everything that

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the researchers asked of them and were rewarded with improved health
and vitality. On average, their total cholesterol dropped from 227 mg/dL
to 172 mg/dL, and their "bad" LDL cholesterol dropped from 152 mg/
dL to 95 mg/dL. And after one year, the frequency, duration and sever-
ity of their chest pains plummeted. Further, it was clear that the closer
the patients adhered to the lifestyle recommendations, the more their
hearts healed. The patients who had the best adherence over the course
of the year saw the blockages in their arteries diminish by over 4%. Four
percent may seem like a small number, but remember that heart disease
builds up over a lifetime, so a 4% change in only a year is a fantastic
result. In all, 82% of the patients in the experimental group had regression
in their heart disease over the course of a year.

The control group did not fare so well, despite the fact that they re-
ceived the usual care. Their chest pain became worse in terms of frequen-
cy, duration and severity. For example, although the experimental group
experienced a 91% reduction in the frequency of chest pain, the control
group experienced a 165% rise in the frequency of chest pain. Their cho-
lesterol levels were significandy worse than those of the experimental pa-
tients, and the blockages in their arteries also became worse. The patients
in the group who were the least attentive to diet and lifestyle changes had
blockages that increased in size by 8% over the course of the year. 46

Between Dr. Ornish, Dr. Esselstyn and others before them, like Dr.
Morrison, I believe that we have found the strategic link in our heart
disease battle plan. Their dietary treatments not only relieve the symp-
toms of chest pain, but they also treat the cause of heart disease and
can eliminate future coronary events. There are no surgical or chemical
heart disease treatments, at the Cleveland Clinic or anywhere else, that
can compare to these impressive results.

THE FUTURE

The future is filled with hope. We now know enough to nearly eliminate
heart disease. We know not only how to prevent the disease, but how to
successfully treat it. We do not need to crack open our breast plates to
reroute our arteries, and we do not need a lifetime of powerful drugs in
our blood. By eating the right food, we can keep our hearts healthy.

The next step is to implement this dietary approach on a large scale,
which is exactly what Dr. Dean Ornish is currently working on. His
research group has begun the Multicenter Lifestyle Demonstration
Project, which represents the future of heart disease health care. Teams

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131

of health professionals at eight diverse sites have been trained to treat
heart disease patients with Dr. Ornish's lifestyle intervention program.
Patients eligible to participate are those who have documented heart
disease severe enough to warrant surgery. Instead of surgery, they may
enroll in a one-year lifestyle program. This program was started in 1993,
and by 1998 there were forty insurance programs that covered the costs
for selected patients. 32

As of 1998, almost 200 people had taken part in the Lifestyle Project,
and the results are phenomenal. After one year of treatment, 65% of
patients had eliminated their chest pain. The effect was long lasting, as
well. After three years, over 60% of the patients continued reporting no
chest pain. 32

The health benefits are equaled by the economic benefits. Over one
million heart disease surgeries are undertaken every year. 32 In 2002,
physician services and hospital care for heart disease patients cost $78.1
billion (that does not include drug costs, home health care or nursing
home care). 2 The angioplasty procedure alone costs $31,000, and by-
pass surgery costs $46,000. 32 In marked contrast, the year-long lifestyle
intervention program only costs $7,000. By comparing the patients who
underwent the lifestyle program with those patients who underwent
the traditional route of surgery, Dr. Ornish and his colleagues demon-
strated that the lifestyle intervention program cut costs by an average of
$30,000 per patient. 32

Much work remains to be done. The health care establishment is
structured to profit from chemical and surgical intervention. Diet still
takes the back seat to drugs and surgery. One criticism that is constantly
leveled at the dietary argument is that patients will not make such funda-
mental changes. One doctor charges that Dr. Esselstyn's patients change
their eating habits simply because of Esselstyn's "zealous belief." 47 This
criticism is not only wrong and insulting to patients; it is also self-fulfill-
ing. If doctors do not believe that patients will change their diets, they
will neglect to talk about diet, or will do it in an off-handed, disparaging
way. There is no greater disrespect a doctor can show patients than that
of withholding potentially lifesaving information based on the assump-
tion that patients do not want to change their lifestyle.

Well-meaning institutions are not exempt from such closed-mind-
edness. The American Heart Association recommends a diet for heart
disease that favors moderation, rather than scientific truth. The National
Cholesterol Education Program does the same thing. These organizations

132

THE CHINA STUDY

pitch moderate diets with trivial changes as being healthy lifestyle "goals."
If you are at high risk for heart disease, or if you already have the disease,
they recommend that you adopt a diet containing 30% of total calories
as fat (7% of total calories as saturated fat) and less than 200 mg/day of
dietary cholesterol. 48,49 According to them, we should also keep our total
blood cholesterol level under the "desirable" level of 200 mg/dL. 49

These venerable organizations are not giving the American public the
most up-to-date scientific information. While we are told that a total
blood cholesterol level of 200 mg/dL is "desirable," we know that 35%
of heart attacks strike Americans who have cholesterol levels between 150
and 200 mg/dL 50 (a truly safe cholesterol level is under 150 mg/dL). We
also know that the most aggressive reversal of heart disease ever dem-
onstrated occurred when fat was about 10% of total calorie intake. Stud-
ies have clearly demonstrated that many patients who follow the more
moderate government recommended diets see a progression of heart
disease. 51 The innocent victims are health-conscious Americans who
follow these recommendations, keeping their total cholesterol around
180 or 190 mg/dL, only to be rewarded with a heart attack leading to a
premature death.

To top it off, the National Cholesterol Education Program danger-
ously writes, "Lifestyle changes are the most cost-effective means to re-
duce risk for CHD [coronary heart disease] . Even so, to achieve maximal
benefit, many persons will require LDL [cholesterol] -lowering drugs." 49
No wonder America's health is failing. The dietary recommendations
for the most diseased hearts among us, given by supposedly reputable
institutions, are severely watered down and followed by the caveat that
we'll probably need a lifetime of drugs anyway

Our leading organizations fear that if they advocate more than mod-
est changes, no one will listen to them. But the establishment-recom-
mended diets are not nearly as healthy as the diets espoused by Drs.
Esselstyn and Ornish. The fact is that a blood cholesterol level of 200
mg/dL is not safe, a 30% fat diet is not "low-fat," and eating foods con-
taining any cholesterol above 0 mg is unhealthy. Our health institutions
are intentionally misleading the public about heart disease, all in the
name of "moderation."

Whether scientists, doctors and policy makers think the public will
change or not, the layperson must be aware that a whole foods, plant-
based diet is far and away the healthiest diet. In the seminal paper re-
garding the landmark Lifestyle Heart Trial, the authors, Dr. Ornish and

BROKEN HEARTS

133

his scientific colleagues, write, "The point of our study was to determine
what is true, not what is practicable [my emphasis]." 46

We now know what is true: a whole foods, plant-based diet can pre-
vent and treat heart disease, saving hundreds of thousands of Americans
every year.

Dr. William Castelli, the long-time director of the Framingham Heart
Study, a cornerstone of heart disease research, espouses a whole foods,
plant-based diet.

Dr. Esselstyn, who has demonstrated the most significant reversal of
heart disease in all of medical history, espouses a whole foods, plant-
based diet.

Dr. Ornish, who has pioneered reversal of heart disease without
drugs or surgery and proved widespread economic benefit for patients
and insurance providers, espouses a whole foods, plant-based diet.

Now is a time of great hope and challenge, a time when people can
control their health. One of the best and most caring doctors I have ever
met puts it best:

The collective conscience and will of our profession
is being tested as never before. Now is the time
for us to have the courage for legendary work.

— Dr. Caldwell B. Esselstyn, Jr. 8

Obesity

Perhaps you've heard the news.

Perhaps you've caught a glimpse of the staggering statistics on obe-
sity among Americans.

Perhaps you've simply noticed that, compared to a few years ago,
more people at the grocery store are overweight.

Perhaps you've been in classrooms, on playgrounds or at day care
centers and noticed how many kids are already crippled with a weight
problem and can't run twenty feet without getting winded.

Our struggle with weight is hard to miss these days. Open a newspa-
per or a magazine, or turn on the radio or TV — you know that America
has a weight problem. In fact, two out of three adult Americans are
overweight, and one-third of the adult population is obese. Not only
are these numbers high, but the rate at which they have been rising is
ominous (Chart 1.2, page 13). 1

But what do the terms "overweight" and "obese" mean? The standard
expression of body size is the body mass index (BMI). It represents body
weight (in kilograms, kg) relative to body height (in meters squared,
m 2 ). By most official standards, being overweight is having a BMI above
twenty-five, and being obese is having a BMI over thirty. The same scale
is used for both men and women. You can determine your own BMI
using Chart 6.1, which lists the necessary information in pounds and
inches for your convenience.

135

136 THE CHINA STUDY

CHART 6.1 : BODY MASS INDEX TABLE

Normal

Overweight

Obese

BMI

[kg/m]

Height
I'm 1

Weight (lb.]

100

105

1 10

1 15

1 19

1 24

129

134

138

143

167

191

104

109

1 14

1 1 9

124

128

133

138

1 43

148

173

198

102

107

1 1 2

1 1 8

1 23

128

133

1 38

143

148

153

1 79

204

1 00

1 06

1 1 1

1 1 6

1 22

1 27

1 32

1 37

1 43

1 48

1 53

158

1 85

21 1

1 04

1 09

1 15

1 20

1 26

1 3 1

1 36

142

1 47

1 53

158

1 64

191

218

1 07

1 1 3

1 1 8

124

1 30

1 35

141

1 46

152

158

163

1 69

197

225

1 10

1 1 6

1 22

128

1 34

1 40

145

1 5 1

1 57

163

169

174

204

232

1 1 4

1 20

1 26

1 32

1 38

1 44

150

1 56

162

168

1 74

1 80

210

240

1 1 8

1 24

1 30

1 36

142

1 48

155

161

167

1 73

1 79

1 86

216

247

121

127

134

140

146

153

159

166

1 72

1 78

185

191

223

255

125

131

138

144

151

158

164

171

177

184

190

197

230

262

128

135

142

149

155

162

169

176

182

189

196

203

236

270

132

139

146

153

160

167

174

181

188

195

202

209

243

278

136

143

150

157

165

172

179

186

193

200

208

215

250

286

140

147

154

162

169

177

184

191

199

206

213

221

258

294

144

151

159

166

174

182

189

197

204

212

219

227

265

302

148

155

163

171

179

186

194

202

210

218

225

233

272

311

152

160

168

176

184

192

200

208

216

224

232

240

279

319

156

164

172

180

189

197

205

213

22]

230

238

246

287

328

THE CHILDREN

Perhaps the most depressing element of our supersize mess is the grow-
ing number of overweight and obese children. About 15% of America's
youth (ages six to nineteen) are overweight. Another 15% are at risk of
becoming overweight. 2

Overweight children face a wide range of psychological and social
challenges. As you know, children have a knack for being open and

OBESITY

137

blunt; sometimes the playground can be a merciless place. Overweight
children find it more difficult to make friends and are often thought of
as lazy and sloppy. They are more likely to have behavioral and learning
difficulties, and the low self-esteem likely to be formed during adoles-
cence can last forever. 3

Young people who are overweight also are highly likely to face a host
of medical problems. They often have elevated cholesterol levels, which
can be a predictor for any number of deadly diseases. They are more
likely to have problems with glucose intolerance, and, consequently,
diabetes. Type 2 diabetes, formerly seen only in adults, is skyrocketing
among adolescents. (See chapters seven and nine for a more thorough
discussion of childhood diabetes.) Elevated blood pressure is nine times
more likely to occur among obese kids. Sleep apnea, which can cause
neuro-cognitive problems, is found in one in ten obese children. A wide
variety of bone problems is more common in obese kids. Most impor-
tantly, an obese young person is much more likely to be an obese adult, 3
greatly increasing the likelihood of lifelong health problems.

CONSEQUENCES FOR THE ADULT

If you 'are obese, you may not be able to do many things that could make
your life more enjoyable. You may find that you cannot play vigorously
with your grandchildren (or your children), walk long distances, par-
ticipate in sports, find a comfortable seat in a movie theatre or airplane
or have an active sex life. In fact, even sitting still in a chair may be im-
possible without experiencing back or joint pain. For many, standing is
hard on the knees. Carrying around too much weight can dramatically
affect physical mobility, work, mental health, self-perception and social
life. So you see, this isn't about death; it really is about missing many of
the more enjoyable things in life. 4

Clearly no one desires to be overweight. So why is it that two out of
three adult Americans are overweight? Why is one-third of the popula-
tion obese?

The problem is not a lack of money. In 1999, medical care costs relat-
ing to obesity alone were estimated to be $70 billion. 5 In 2002, a mere
three years later, the American Obesity Association listed these costs at
$100 billion. 6 This is not all. Add another $30-40 billion out-of-pocket
money that we spend trying to keep off the weight in the first place. 5
Going on special weight-loss diet plans and popping pills to cut our ap-
petites or rearrange our metabolism have become a national pastime.

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THE CHINA STUDY

This is an economic black hole that sucks our money away without
offering anything in return. Imagine paying $40 to a service man to
fix your leaky kitchen sink, and then two weeks later, the sink pipes
explode and flood the kitchen and it costs $500 to repair. I bet you
wouldn't ask that guy to fix your sink again! So then why do we end-
lessly try those weight-loss plans, books, drinks, energy bars and as-
sorted gimmicks when they don't deliver as promised?

I applaud people for trying to achieve a healthy weight. I don't ques-
tion the worthiness or dignity of overweight people any more than I
question cancer victims. My criticism is of a societal system that allows
and even encourages this problem. I believe, for example, that we are
drowning in an ocean of very bad information, too much of it intended
to put money into someone else's pockets. What we really need, then, is
a new solution comprised of good information for individual people to
use at a price that they can afford.

THE SOLUTION

The solution to losing weight is a whole foods, plant-based diet, cou-
pled with a reasonable amount of exercise. It is a long-term lifestyle
change, rather than a quick-fix fad, and it can provide sustained weight
loss while minimizing risk of chronic disease.

Have you ever known anyone who regularly consumes fresh fruits,
vegetables and whole grain foods — and rarely, if ever, consumes meats
or junk foods like chips, French fries and candy bars? What is his or her
weight like? If you know many people like this, you have probably no-
ticed that they tend to have a healthy weight. Now think of traditional
cultures around the world. Think of traditional Asian cultures (Chinese,
Japanese, Indian), where a couple of billion people have been eating a
mostly plant-based diet for thousands of years. It's hard to imagine these
people — at least until recently — as anything other than slender.

Now imagine a guy buying two hot dogs and ordering his second beer
at a baseball game, or a woman ordering a cheeseburger and fries at your
local fast food joint. The people in these images look different, don't they?
Unfortunately, the guy munching his hot dogs and sipping his beer is rap-
idly becoming the "all-American" image. I have had visitors from other
countries tell me that one of the first things they notice when they arrive
in our good land is the exceptional number of fat people.

Solving this problem does not require magic tricks or complex
equations involving blood types or carbohydrate counting or soul

OBESITY

139

searching. Simply trust your observations on who is slim, vigorous
and healthy and who is not. Or trust the findings of some impres-
sive research studies, large and small, showing time and time again
that vegetarians and vegans are slimmer than their meat-eating
counterparts. People in these studies who are vegetarian or vegan
are anywhere from five to thirty pounds slimmer than their fellow citi-
zens. 7-13

In a separate intervention study, overweight subjects were told to
eat as much as they wanted of foods that were mostly low-fat, whole-
food and plant-based. In three weeks these people lost an average of
seventeen pounds. 14 At the Pritikin Center, 4,500 patients who had
gone through their three-week program got similar results. By feeding a
mostly plant-based diet and promoting exercise, the Center found that
its clients lost 5.5% of their body weight over three weeks. 15

Published results for still more intervention studies using a low-fat,
whole foods, mostly plant-based diet:

• About two to five pounds lost after twelve days 16

• About ten pounds lost in three weeks 17 ' 18

• Sixteen pounds lost over twelve weeks 19

• Twenty-four pounds lost after one year 20

All of these results show that consuming a whole foods, plant-based
diet will help you to lose weight and, furthermore, it can happen quick-
ly. The only question is how much weight you can lose. In most of these
studies, the people who shed the most pounds were those who started
with the most excess weight. 21 After the initial weight loss, the weight
can be kept off for the long term by staying on the diet. Most impor-
tantly, losing weight this way is consistent with long-term health.

Some people, of course, can be on a plant-based diet and still not lose
weight. There are a few very good reasons for this. First and foremost,
losing body weight on a plant-based diet is much less likely to occur if
the diet includes too many refined carbohydrates. Sweets, pastries and
pastas won't do it. These foods are high in readily digested sugars and
starches and, for the pastries, oftentimes very high in fat as well. As
mentioned in chapter four, these highly processed, unnatural foods are
not part of a plant-based diet that works to reduce body weight and pro-
mote health. This is one of the main reasons that I usually refer to the
optimal diet as a wholefoods, plant-based diet.

Notice that a strict vegetarian diet is not necessarily the same thing

140

THE CHINA STUDY

as a whole foods, plant-based diet. Some people become vegetarian only
to replace meat with dairy foods, added oils and refined carbohydrates,
including pasta made with refined grains, sweets and pastries. I refer to
these people as "junk-food vegetarians" because they are not consum-
ing a nutritious diet.

The second reason weight loss may be elusive is if a person never en-
gages in any physical activity. A reasonable amount of physical activity,
sustained on a regular basis, can pay important dividends.

Thirdly, certain people have a family predisposition for overweight
bodies that may make their challenge more difficult. If you are one of
these people, I can only say that you probably need to be especially rig-
orous in your diet and exercise. In rural China, we noticed that obese
people simply did not exist, even though Chinese immigrants in West-
ern countries do succumb to obesity. Now, as the dietary and lifestyle
practices of people in China are becoming more like ours, so too have
their bodies become more like ours. For some of these people with ge-
netic predispositions, it doesn't take much bad food before their change
in diet starts to cause problems.

Keeping body weight off is a long-term lifestyle choice. Gimmicks
that produce impressively large, quick weight losses don't work in the
long term. Short-term gains should not come along with long-term pain,
like kidney problems, heart disease, cancer, bone and joint ailments
and other problems that may be brought on with popular diet fads. If
the weight was gained slowly, over a period of months and years, why
would you expect to take it off healthily in a matter of weeks? Treating
weight loss as a race doesn't work; it only makes the dieter more eager
to quit the diet and go back to the eating habits that put them in need
of losing weight in the first place. One very large study of 21,105 veg-
etarians and vegans 13 found that body mass index was ". . . lower among
those who had adhered to their diet for five or more years" compared to
people who had been on the diet for less than five years.

WHY THIS WILL WORK FOR YOU

So there is a solution to the weight-gain problem. But how can you ap-
ply it to your own life?

First of all, throw away ideas about counting calories. Generally speak-
ing, you can eat as much as you want and still lose weight — as long you
eat the right type of food. (See chapter twelve for details.) Secondly, stop
expecting sacrifice, deprivation or blandness; there's no need. Feeling

OBESITY

141

hungry is a sign that something is wrong, and prolonged hunger causes
your body to slow the overall rate of metabolism in defense. Moreover,
there are mechanisms in our bodies that naturally allow the right kind
of plant-based foods to nourish us, without our having to think about
every morsel of food we put in our mouths. It is a worry-free way to eat.
Give your body the right food and it will do the right thing.

In some studies, those who follow a whole foods, low-fat, plant-based
diet consume fewer calories. It's not because they're starving themselves.
In fact, they will likely spend more time eating and eat a larger volume
of food than their meat-eating counterparts. 22 That's because fruits, veg-
etables and grains — as whole foods — are much less energy-dense than
animal foods and added fats. There are fewer calories in each spoonful
or cupful of these foods. Remember that fat has nine calories per gram
while carbohydrates and protein have only four calories per gram. In
addition, whole fruits, vegetables and grains have a lot of fiber, which
makes you feel full 22 - 23 and yet contributes almost no calories to your
meal. So by eating a healthy meal, you may reduce the calories that you
consume, digest and absorb, even if you eat significantly more food.

This idea on its own, however, is not yet a sufficient explanation
for the benefits of a whole foods, plant-based diet. The same criticisms
I made against the Atkins diet and the other popular "low-carb" di-
ets (chapter four) can also be applied to short-term studies in which
subjects consume fewer calories while eating a plant-based diet. Over
the long term, these subjects will find it very difficult to continue con-
suming an abnormally low level of calories; weight loss due to calorie
restriction rarely leads to long-term weight loss. This is why other stud-
ies play such a crucial part in explaining the health benefits of a whole
foods, plant-based diet, studies that show that the weight-loss effect is
due to more than simple calorie restriction.

These studies document the fact that vegetarians consume the same
amount or even significantly more calories than their meat-eating counter-
parts, and yet are still slimmer. 11 - 2 *- 25 The China Study demonstrated that
rural Chinese consuming a plant-based diet actually consume signifi-
cantly more calories per pound of body weight than Americans. Most
people would automatically assume that these rural Chinese would
therefore be heavier than their meat-eating counterparts. But here's
the kicker: the rural Chinese are still slimmer while consuming a greater
volume of food and more calories. Much of this effect is undoubtedly due
to greater physical activity .. .but this comparison is between average

142

THE CHINA STUDY

Americans and the least active Chinese, those who do office work. Fur-
thermore, studies done in Israel 24 and the United Kingdom, 11 neither of
which represent primarily agrarian cultures, also show that vegetarians
may consume the same or significantly more calories and still weigh
less.

What's the secret? One factor that I've mentioned previously is the
process of thermogenesis, which refers to our production of body heat
during metabolism. Vegetarians have been observed to have a slightly
higher rate of metabolism during rest, 26 meaning they burn up slightly
more of their ingested calories as body heat rather than depositing them
as body fat. 27 A relatively small increase in metabolic rate translates to a
large number of calories burned over the course of twenty-four hours.
Most of the scientific basis for the importance of this phenomenon was
presented in chapter four.

EXERCISE

The slimming effect of physical activity is obvious. Scientific evidence
concurs. A recent review of all the credible studies compared the rela-
tionship between body weight and exercise 28 and showed that people
who were more physically active had less body weight. Another set of
studies showed that exercising on a regular basis helped to keep off
weight originally lost through exercise programs. No surprise here,
either. Starting and stopping an exercise program is not a good idea. It
is better to build it into your lifestyle so that you will become and con-
tinue to be more fit over all, not just burn off calories.

How much exercise is needed to keep the pounds off? A rough es-
timate derived from a good review 28 suggested that exercising a mere
fifteen to forty-five minutes per day, every day, will maintain a body
weight that is eleven to eighteen pounds lighter than it would otherwise
be. Interestingly, we should not forget our "spontaneous" physical activ-
ity, the kind that is associated with chores of daily life. This can account
for 100-800 calories per day (kcal/day). 29 ' 30 People who are regularly
"up and about" doing physical things are going to be well ahead of those
who get trapped in a sedentary lifestyle.

The advantages of combining diet and exercise to control body
weight were brought home to me by a very simple study involving our
experimental animals. Recall that our experimental animals were fed
diets containing either the traditional 20% casein (cow's milk protein)
or the much lower 5% casein. The rats consuming the 5% casein diets

OBESITY

143

had strikingly less cancer, lower blood cholesterol levels and longer
lives. They also consumed slightly more calories but burned them off
as body heat.

Some of us had noticed over the course of these experiments that the
5% casein animals seemed to be more active than the 20% casein ani-
mals. To test this idea, we housed rats fed either 5% or 20% casein diets
in cages equipped with exercise wheels outfitted with meters to record
the number of turns of the wheel. Within the very first day, the 5% casein-
fed animals voluntarily "exercised" in the wheel about twice as much as the
20% casein-fed animals. 31 Exercise remained considerably higher for the
5% casein animals throughout the two weeks of the study.

Now we can combine some really interesting observations on body
weight. A plant-based diet operates on calorie balance to keep body
weight under control in two ways. First, it discharges calories as body
heat instead of storing them as body fat, and it doesn't take many calo-
ries to make a big difference over the course of a year. Second, a plant-
based diet encourages more physical activity. And, as body weight goes
down, it becomes easier to be physically active. Diet and exercise work
together to decrease body weight and improve overall health.

GOING IN THE RIGHT DIRECTION

Obesity is the most ominous harbinger of poor health that Western na-
tions currently face. Tens of millions of people will fall prey to disability
putting our health care systems under greater strain than has previously
been seen.

There are many people and institutions working to reduce this prob-
lem, but their point of attack is often illogical and misinformed. First,
there are the many quick-fix promises and gimmicks. Obesity is not a
condition that can be fixed in a few weeks or even a few months, and
you should beware of diets, potions and pills that create rapid weight
loss with no promise of good health in the future. The diet that helps to
reduce weight in the short run needs to be the same diet that creates and
maintains health in the long run.

Second, the tendency to focus on obesity as an independent, isolated
disease 32, 33 is misplaced. Considering obesity in this manner directs our
attention to a search for specific cures while ignoring control of the other
diseases to which obesity is strongly linked. That is, we sacrifice context.

Also, I would urge that we ignore the suggestion that knowing its
genetic basis might control obesity. A few years ago, 34 36 there was great

144

THE CHINA STUDY

publicity given to the discovery of "the obesity gene." Then there was
the discovery of a second gene related to obesity and a third gene, and
a fourth and on and on. The purpose behind the obesity gene search is
to allow researchers to develop a drug capable of knocking out or inac-
tivating the underlying cause of obesity. This is extremely shortsighted,
as well as unproductive. Believing that specific identifiable genes are the
basis of obesity (i.e., it's all in the family) also allows us to fatalistically
blame a cause that we cannot control.

We can control the cause. It is right at the end of our fork.

Diabetes

Type 2 diabetes, the most common form, often accompanies obesity. As
we, as a nation, continue to gain weight, our rate of diabetes spirals out
of control. In the eight years from 1990 to 1998, the incidence of diabe-
tes increased 33%. 1 Over 8% of American adults are diabetic, and over
150,000 young people have the disease. That translates to 16 million
Americans. The scariest figure? One-third of those people with diabetes
don't yet know that they have it. 2

You know the situation is serious when our children, at the age of
puberty, start falling prey to the form of diabetes usually reserved for
adults over forty. One newspaper recently illustrated the epidemic with
the story of a girl who weighed 350 pounds at the age of fifteen, had the
"adult-onset" form of diabetes and was injecting insulin into her body
three times a day 3

What is diabetes, why should we care about it and how do we stop it
from happening to us?

TWO FACES OF THE SAME DEVIL

Almost all cases of diabetes are either Type 1 or Type 2. Type 1 develops
in children and adolescents, and thus is sometimes referred to as juve-
nile-onset diabetes. This form accounts for 5% to 10% of all diabetes
cases. Type 2, which accounts for 90% to 95% of all cases, used to occur
primarily in adults age forty and up, and thus was called adult-onset
diabetes. 2 But because up to 45% of new diabetes cases in children are
Type 2 diabetes, 4 the age-specific names are being dropped, and the two
forms of diabetes are simply referred to as Type 1 and Type 2. 4

145

146

THE CHINA STUDY

In both types, the disease begins with dysfunctional glucose metabo-
lism. Normal metabolism goes like this:

• We eat food.

• The food is digested and the carbohydrate part is broken down
into simple sugars, much of which is glucose.

• Glucose (blood sugar) enters the blood, and insulin is produced by
the pancreas to manage its transport and distribution around the
body.

• Insulin, acting like an usher, opens doors for glucose into different
cells for a variety of purposes. Some of the glucose is converted to
short-term energy for immediate cell use, and some is stored as
long-term energy (fat) for later use.

As a person develops diabetes, this metabolic process collapses. Type
1 diabetics cannot produce adequate insulin because the insulin-pro-
ducing cells of their pancreas have been destroyed. This is the result
of the body attacking itself, making Type 1 diabetes an autoimmune
disease. (Type 1 diabetes and other autoimmune diseases are discussed
in chapter nine.) Type 2 diabetics can produce insulin, but the insulin
doesn't do its job. This is called insulin resistance, which means that
once the insulin starts "giving orders" to dispatch the blood sugar, the
body doesn't pay attention. The insulin is rendered ineffective, and the
blood sugar is not metabolized properly.

Imagine your body as an airport, complete with vast parking areas.
Each unit of your blood sugar is an individual traveler. After you eat,
your blood sugar rises. In our analogy, then, that means lots of travel-
ers would start to arrive at the airport. The people would drive in, park
in a lot and walk to the stop where the shuttle bus is supposed to pick
them up. As your blood sugar continues to rise, all the airport parking
lots would fill to capacity, and all the people would congregate at the
shuttle bus stops. The shuttle buses, of course, represent insulin. In the
diabetic airport, unfortunately, there are all sorts of problems with the
buses. In the Type 1 diabetic airport, the shuttle buses simply don't ex-
ist. The only shuttle bus manufacturer in the known universe, Pancreas
Company, was shut down. In the Type 2 diabetic airport, there are some
shuttle buses, but they don't work very well.

In both cases, travelers never get to where they want to go. The
airport system breaks down, and chaos ensues. In real life, this corre-
sponds with a rise in blood sugar to dangerous levels. In fact, diabetes

DIABETES

147

is diagnosed by the observation of elevated blood sugar levels, or its
"spillage" into urine.

What are the long-term health risks of glucose metabolism being
disrupted? Here's a summary, taken from a report from the Centers for
Disease Control 2 :

Diabetes Complications

Heart Disease

• 2-4 times the risk of death from heart disease.
Stroke

• 2-4 times the risk of stroke.

High Blood Pressure

• Over 70% of people with diabetes have high blood pressure.

Blindness

• Diabetes is the leading cause of blindness in adults.

Kidney Disease

• Diabetes is the leading cause of end-stage kidney disease.

• Over 100,000 diabetics underwent dialysis or kidney trans-
plantation in 1999.

Nervous System Disease

• 60% to 70% of diabetics suffer mild to severe nervous system
damage.

Amputation

• Over 60% of all lower limb amputations occur with diabet-
ics.

Dental Disease

• Increased frequency and severity of gum disease that can lead
to tooth loss.

Pregnancy Complications

Increased Susceptibility to Other Illnesses

Death

148

THE CHINA STUDY

Modern drugs and surgery offer no cure for diabetics. At best, current
drugs allow diabetics to maintain a reasonably functional lifestyle, but
these drugs will never treat the cause of the disease. As a consequence,
diabetics face a lifetime of drugs and medications, making diabetes an
enormously costly disease. The economic toll of diabetes in the U.S.:
over $130 billion a year. 2

But there is hope. In fact, there is much more than hope. The food
we eat has enormous influence over this disease. The right diet not only
prevents but also treats diabetes. What, then, is the "right" diet? You
can probably guess what I'm going to say but let the research speak for
itself.

NOW YOU SEE IT, NOW YOU DON'T

Like most chronic diseases, diabetes shows up more often in some parts
of the world than in others. This has been known for a hundred years.
It has also been well documented that those populations with low rates
of diabetes eat different diets than those populations with high rates
of diabetes. But is that just a coincidence, or is there something else at
work?

CHART 7.1: DIETS AND DIABETES RATES, CIRCA 1925" 5

l % Fat

I % Carbohydrates
■Diabetes

DIABETES

149

Almost seventy years ago, H.P. Himsworth compiled all the existing
research in a report comparing diets and diabetes rates in six countries.
What he found was that some cultures were consuming high-fat diets,
while others had diets high in carbohydrates. These fat vs. carbohydrate
consumption patterns were the result of animal vs. plant food consump-
tion. Chart 7.1 documents the diet and disease conditions for these
countries in the early part of the twentieth century. 5

As carbohydrate intake goes up and fat intake goes down, the num-
ber of deaths from diabetes plummets from 20.4 to 2.9 per 100,000
people. The verdict? A high-carbohydrate, low-fat diet — a plant-based
diet — may help to prevent diabetes.

Thirty years later, the question was reexamined. After examining four
countries from Southeast Asia and South America, researchers again
found that high-carbohydrate diets were linked to low rates of diabetes.
Researchers noted that the country with the highest rate of diabetes,
Uruguay, had a diet that was "typically 'Western' in character, being
high in calories, animal protein, [total] fat and animal fat." Countries
with low rates of diabetes used a diet that was "relatively lower in pro-
tein (particularly animal protein), fat and animal fat. A high proportion
of calories is derived from carbohydrates, particularly from rice." 6

These same researchers enlarged their study to eleven countries
through Central and South America and Asia. The strongest associa-
tion they found with diabetes was excess weight. 7 Populations eating
the most "Western" type of diet also had the highest cholesterol levels,
which in turn was strongly associated with the rate of diabetes. 7 Is this
starting to sound familiar?

WITHIN ONE POPULATION

These old, cross-cultural studies can be crude, resulting in conclusions
that are not entirely reliable. Perhaps the difference in diabetes rates in
the above studies were not due to diet, but to genetics. Perhaps other
unmeasured cultural factors, like physical activity, were more relevant.
A better test would be a study of diabetes rates in a single population.

The Seventh-day Adventists population is a good example. They are
an interesting group of people to study because of their dietary habits:
their religion encourages them to stay away from meat, fish, eggs, cof-
fee, alcohol and tobacco. As a result, half of them are vegetarian. But
90% of these vegetarians still consume dairy and/or egg products, thus
deriving a significant amount of their calories from animal sources. It

150

THE CHINA STUDY

should also be noted that the meat-eating Adventists are not the meati-
est of eaters. They consume about three servings of beef a week, and less
than one serving a week of fish and poultry. 8 I know plenty of people
who consume this amount of meat (including fish and poultry) every
two days.

In dietary studies involving the Adventists, scientists compare "mod-
erate" vegetarians to "moderate" meat eaters. This is not a big differ-
ence. Even so, the Adventist vegetarians are much healthier than their meat
eating counterparts. 8 Those Adventists that "deprived" themselves of meat
also "deprived" themselves of the ravages of diabetes. Compared to the meat
eaters, the vegetarians had about one-half the rate of diabetes. 8 9 They also
had almost half the rate of obesity. 8

In another study, scientists measured diets and diabetes in a popula-
tion of Japanese American men in Washington State. 10 These men were
the sons of Japanese immigrants to the U.S. Remarkably, they had more
than four times the prevalence of diabetes than the average rate found in
similar-aged men who stayed in Japan. So what happened?

For Japanese Americans, the ones who developed diabetes also ate
the most animal protein, animal fat and dietary cholesterol, each of
which is only found in animal-based foods. 10 Total fat intake also was
higher among the diabetics. These same dietary characteristics also re-
sulted in excess weight. These second-generation Japanese Americans
ate a meatier diet with less plant-based food than men born in Japan.
The researchers wrote, "Apparently, the eating habits of Japanese men
living in the United States resemble more the American eating style
than the Japanese." The consequence: four times as much incidence of
diabetes. 10

Some other studies:

• Researchers found that increased fat intake was associated with an
increased rate of Type 2 diabetes among 1 ,300 people in the San
Luis valley in Colorado. They said, "The findings support the hy-
pothesis that high-fat, low-carbohydrate diets are associated with
the onset of non-insulin-dependent [Type 2] diabetes mellitus in
humans." 11

• In the past twenty-five years, the rate at which children in Japan
contract Type 2 diabetes has more than tripled. Researchers note
that consumption of animal protein and animal fat has drastically
increased in the past fifty years. Researchers say that this dietary

DIABETES

151

shift, along with low exercise levels, might be to blame for this
explosion of diabetes. 12

• In England and Wales the rate of diabetes markedly dropped from
1940 to 1950, largely during World War II when food consump-
tion patterns changed markedly. During the war and its aftermath,
fiber and grain intake went up and fat intake went down. People
ate "lower" on the food chain because of national necessity Around
1950, though, people gave up the grain-based diets and returned
to eating more fat, more sugar and less fiber. Sure enough, diabetes
rates started going up. 13

• Researchers studied 36,000 women in Iowa for six years. All were
free of diabetes at the start of the study, but more than 1,100 cases
of diabetes developed after six years. The women who were least
likely to get diabetes were those that ate the most whole grains and
fiber 14 — those whose diets contained the most carbohydrates (the
complex kind found in whole foods).

All of these findings support the idea that both across and within
populations, high-fiber, whole, plant-based foods protect against diabe-
tes, and high-fat, high-protein, animal-based foods promote diabetes.

CURING THE INCURABLE

All of the research cited above was observational and an observed as-
sociation, even if frequently seen, may only be an incidental association
that masks the real cause-effect relationship of environment (including
diet) and disease. There is, however, also research of the "controlled"
or intervention variety This involves changing the diets of people who
already have either full-blown Type 1 or Type 2 diabetes or mild diabetic
symptoms (impaired glucose tolerance).

James Anderson, M.D., is one of the most prominent scientists study-
ing diet and diabetes today, garnering dramatic results using dietary
means alone. One of his studies examined the effects of a high-fiber,
high-carbohydrate, low-fat diet on twenty-five Type 1 diabetics and
twenty- five Type 2 diabetics in a hospital setting. 15 None of his fifty
patients were overweight and all of them were taking insulin shots to
control their blood sugar levels.

His experimental diet consisted mostly of whole plant foods and the
equivalent of only a cold cut or two of meat a day. He put his patients on
the conservative, American-style diet recommended by the American

152

THE CHINA STUDY

Diabetes Association for one week and then switched them over to the
experimental "veggie" diet for three weeks. He measured their blood
sugar levels, cholesterol levels, weight and medication requirements.
The results were impressive.

Type 1 diabetics cannot produce insulin. It is difficult to imagine
any dietary change that might aid their predicament. But after just
three weeks, the Type 1 diabetic patients were able to lower their insulin
medication by an average of 40%! Their blood sugar profiles improved
dramatically Just as importantly, their cholesterol levels dropped by 30%/ 15
Remember, one of the dangers of being diabetic is the secondary out-
comes, heart disease and stroke. Lowering risk factors for those second-
ary outcomes by improving the cholesterol profile is almost as impor-
tant as treating high blood sugar.

Type 2 diabetics, unlike Type 1, are more "treatable" because they
haven't incurred such extensive damage to their pancreas. So when An-
derson's Type 2 patients ate the high-fiber, low-fat diet, the results were
even more impressive. Of the twenty-five Type 2 patients, twenty-four
were able to discontinue their insulin medication! Let me say that again.
All but one person were able to discontinue their insulin medication in a mat-
ter of weeks! 15

One man had a twenty-one-year history of diabetes and was taking
thirty-five units of insulin a day. After three weeks of intensive dietary
treatment, his insulin dosage dropped to eight units a day. After eight
weeks at home, his need for insulin shots vanished. 15 Chart 7.2 shows
a sample of patients and how eating a plant-based diet lowered their
insulin medications. This is a huge effect.

In another study of fourteen lean diabetic patients, Anderson found
that diet alone could lower total cholesterol levels by 32% in just over
two weeks. 16 Some of the results are shown in Chart 7.3.

These benefits, representing a decrease in blood cholesterol from 206
mg/dL to 141 mg/dL, are astounding — especially considering the speed
with which they appear. Dr. Anderson also found no evidence that this
cholesterol decrease was temporary as long as people continued on the
diet; it remained low for four years. 17

Another group of scientists at the Pritikin Center achieved equally
spectacular results by prescribing a low-fat, plant-based diet and exer-
cise to a group of diabetic patients. Of forty patients on medication at the
start oj the program, thirty-jour were able to discontinue all medication
after only twenty-six days. 18 This research group also demonstrated that

DIABETES

153

30 |—

CHART 7.2: INSULIN DOSAGE RESPONSE TO DIET

HCF DIET
(High-Carbohydrate,
High-Fiber Diet)

N = 8

the benefits of a plant-based diet will last for years if the same diet is
continued. 19

These are examples of some very dramatic research, but they only
scratch the surface of all the supporting research that has been done.
One scientific paper reviewed nine publications citing the use of high-
carbohydrate, high-fiber diets and two more standard-carbohydrate,
high-fiber diets to treat diabetic patients. 20 All eleven studies resulted
in improved blood sugar and cholesterol levels. (Dietary fiber supple-
ments, by the way although beneficial, did not have same consistent
effects as a change to a plant-based, whole foods diet.) 21

THE PERSISTENCE OF HABIT

As you can see by these findings, we can beat diabetes. Two recent
studies considered a combination of diet and exercise effects on this
disease. 22, 23 One study placed 3,234 non-diabetic people at risk for dia-
betes (elevated blood sugar) into three different groups. 22 One group,
the control, received standard dietary information and a drug placebo
(no effect), one received the standard dietary information and the drug
metformin, and a third group received "intensive" lifestyle intervention,
which included a moderately low-fat diet and exercise plan to lose at
least 7% of their weight. After almost three years, the lifestyle group had

154

THE CHINA STUDY

CHART 7.3: BLOOD CHOLESTEROL ON HIGH-CARBOHYDRATE,
HIGH-FIBER DIET

o 80

CONTROL

HCF DIET

(High-Carbohydrate,

High-Fiber Diet)

N = 14

Type 1 Patients

CHOLESTEROL

-6 0 6 12 18

Days

58% fewer cases of diabetes than the control group. The drug group re-
duced the number of cases only by 31%. Compared to the control, both
treatments worked, but clearly a lifestyle change is much more power-
ful and safer than simply taking a drug. Moreover, the lifestyle change
would be effective in solving other health problems, whereas the drug
would not.

The second study also found that the rate of diabetes could be re-
duced by 58% just by modest lifestyle changes, including exercise,
weight loss and a moderately low-fat diet. 23 Imagine what would hap-
pen if people fully adopted the healthiest diet: a whole foods, plant-
based diet. I strongly suspect that virtually all Type 2 diabetes cases
could be prevented.

Unfortunately, misinformation and ingrained habits are wreaking
havoc on our health. Our habit of eating hot dogs, hamburgers and
French fries is killing us. Even Dr. James Anderson, who achieved pro-
found results with many patients by prescribing a near-vegetarian diet,
is not immune to habitual health advice. He writes, "Ideally diets pro-
viding 70% of calories as carbohydrate and up to 70 gm fiber daily offer
the greatest health benefits for individuals with diabetes. However, these
diets allow only one to two ounces of meat daily and are impractical for
home use for many individuals." 20 Why does Professor Anderson, a very

DIABETES

155

fine researcher, say that such a diet is "impractical" and thereby preju-
dice his listeners before they even consider the evidence?

Yes, changing your lifestyle may seem impractical. It may seem im-
practical to give up meat and high-fat foods, but I wonder how practical
it is to be 350 pounds and have Type 2 diabetes at the age of fifteen, like
the girl mentioned at the start of this chapter. I wonder how practical it
is to have a lifelong condition that can't be cured by drugs or surgery; a
condition that often leads to heart disease, stroke, blindness or amputa-
tion; a condition that might require you to inject insulin into your body
every day for the rest of your life.

Radically changing our diets may be "impractical," but it might also
be worth it.

Common Cancers:
Breast Prostate, Large Bowel
(Colon and Rectal)

Much of my career has been concentrated on the study of cancer. My
laboratory work was focused on several cancers, including those of the
liver, breast and pancreas, and some of the most impressive data from
China were related to cancer. For this lifetime work, the American In-
stitute for Cancer Research kindly presented me with their Research
Achievement award in 1998.

An exceptional number of books have summarized the evidence on
the effects of nutrition on a variety of cancers, each with their own
particularities. But what I've found is that the nutritional effects on the
cancers I've chosen to discuss here are virtually the same for all cancers,
regardless of whether they are initiated by different factors or are lo-
cated in different parts of the body. Using this principle, I can limit my
discussion to three cancers, which will allow me space in the rest of the
book to address diseases other than cancer, demonstrating the breadth
of evidence linking food to many health concerns.

I have chosen to comment on three cancers that affect hundreds of
thousands of Americans and that generally represent other cancers as
well: two reproductive cancers that get plenty of attention, breast and

157

158

THE CHINA STUDY

prostate, and one digestive cancer, large bowel — the second leading
cause of cancer death, behind lung cancer.

BREAST CANCER

It was spring almost ten years ago. I was in my office at Cornell when I
was told that a woman with a question regarding breast cancer was on
the phone.

"I have a strong history of breast cancer in my family," the woman,
Betty, said. "My mother and grandmother both died from the disease,
and my forty-five-year-old sister was recently diagnosed with it. Given
this family problem, I can't help but be afraid for my nine-year-old
daughter. She's going to start menstruating soon and I worry about her
risks of getting breast cancer." Her fear was evident in her voice. "I've
seen a lot of research showing that family history is important, and I'm
afraid that it's inevitable that my daughter will get breast cancer. One of
the options I've been thinking about is a mastectomy for my daughter,
to remove both breasts. Do you have any advice?"

This woman was in an exceptionally difficult position. Does she let
her daughter grow up into a deathtrap, or grow up without breasts? Al-
though extreme, this question represents a variety of similar questions
faced every day by thousands of women around the world.

These questions were especially encouraged by the early reports on
the discovery of the breast cancer gene, BRCA-1. Headline articles in the
New York Times and other newspapers and magazines trumpeted this
discovery as an enormous advance. The hoopla surrounding BRCA-1,
which now also includes BRCA-2, reinforced the idea that breast cancer
was due to genetic misfortune. This caused great fear among people
with a family history of breast cancer. It also generated excitement
among scientists and pharmaceutical companies. The possibility was
high that new technologies would be able to assess overall breast cancer
risk in women by doing genetic testing; they hoped they might be able
to manipulate this new gene in a way that would prevent or treat breast
cancer. Journalists busily started translating selective bits of this infor-
mation for the public, relying heavily on the genetic fatalistic attitude.
No doubt this contributed to the concern of mothers like Betty.

"Well, let me first tell you that I am not a physician," I said. "I can't
help you with diagnosis or treatment advice. That's for your physician
to do. I can speak about the current research in a more general way,
however, if that is of any help to you."

COMMON CANCERS: BREAST, PROSTATE, LARGE BOWEL

159

"Yes," she said, "that's what I wanted."

I told her a little bit about the China Study and about the important
role of nutrition. I told her that just because a person has the gene for a
disease does not mean that they are destined to get the cancer: promi-
nent studies reported that only a tiny minority of cancers can be solely
blamed on genes.

I was surprised at how little she knew about nutrition. She thought
genetics was the only factor that determined risk. She didn't realize that
food was an important factor in breast cancer as well.

We talked for twenty or thirty minutes, a brief time for such an impor-
tant matter. By the end of the conversation I had the feeling that she was
not satisfied with what I told her. Perhaps it was my conservative, scientif-
ic way of talking, or my reluctance to give her a recommendation. Maybe,
I thought, she had already made up her mind to do the procedure.

She thanked me for my time and I wished her well. I remember
thinking about how often I receive questions from people about specific
health situations, and that this was one of the most unusual.

But Betty wasn't alone. One other woman also talked to me regarding
the possibility of her young daughter undergoing surgery to remove both
breasts. Other women who already had one breast removed wondered
whether to have the second breast removed as a preventative measure.

It's clear that breast cancer is an important concern in our society.
One out of eight American women will be diagnosed with this disease
during their lifetimes — one of the highest rates in the world. Breast
cancer grassroots organizations are widespread, strong, relatively well
funded and exceptionally active compared to other health activist orga-
nizations. This disease, perhaps more than any other, incites panic and
fear in many women.

When I think back to that conversation I had with Betty, I now feel
that I could have made a stronger statement about the role nutrition
plays in breast cancer. I still would not have been able to give her clini-
cal advice, but the information I now know might have been of more
use to her. So what would I tell her now?

RISK FACTORS

There are at least four important breast cancer risk factors that are af-
fected by nutrition, as shown in Chart 8.1. Many of these relationships
were confirmed in the China Study after being well established in other
research.

160 THE CHINA STUDY

CHART 8.1: BREAST CANCER RISK FACTORS
AND NUTRITIONAL INFLUENCE

Risk of breast cancer increases
when a woman has . . .

A diet high in animal foods
and refined carbohydrates . . .

. . . early age of menarche (first men-
struation)

. . . lowers the age of menarche

. . . late age of menopause

. . . raises the age of menopause

. . . high levels of female hormones in
the blood

. . . increases female hormone levels

. . . high blood cholesterol

. . . increases blood cholesterol levels

With the exception of blood cholesterol, these risk factors are
variations on the same theme: exposure to excess amounts of female
hormones, including estrogen and progesterone, leads to an increased
risk of breast cancer. Women who consume a diet rich in animal-based
foods, with a reduced amount of whole, plant-based foods, reach pu-
berty earlier and menopause later, thus extending their reproductive
lives. They also have higher levels of female hormones throughout their
lifespan, as shown in Chart 8.2.

According to our China Study data, lifetime exposure to estrogen 1 is
at least 2.5-3.0 times higher among Western women when compared

CHART 8.2: DIETARY INFLUENCE ON FEMALE HORMONE EXPOSURE
OVER A WOMAN'S LIFETIME (SCHEMATIC)

— - Plant-Based Diet
^^—Animal-Based Diet

5 10 15 20 25 30 35 40 45 50 55 60

Woman's Age

COMMON CANCERS: BREAST, PROSTATE, LARGE BOWEL

161

with rural Chinese women. This is a huge difference for such a criti-
cally important hormone. 2 To use the words of one of the leading breast
cancer research groups in the world, 3 "there is overwhelming evidence
that estrogen levels are a critical determinant of breast cancer risk." 4 ' 5
Estrogen directly participates in the cancer process. 6, 7 It also tends to
indicate the presence of other female hormones*" 12 that play a role in
breast cancer risk. 6, 7 Increased levels of estrogen and related hormones
are a result of the consumption of typical Western diets, high in fat and
animal protein and low in dietary fiber. 3, 13-18

The difference in estrogen levels between rural Chinese women and
Western women 19 is all the more remarkable because a previous report 20
found that a mere 17% decrease in estrogen levels could account for a
huge difference in breast cancer rates when comparing different coun-
tries. Imagine, then, what 26-63% lower blood estrogen levels and
eight to nine fewer reproductive years of blood estrogen exposure could
mean, as we found in the China Study.

This idea that breast cancer is centered on estrogen exposure 3, 21,22 is
profound because diet plays a major role in establishing estrogen expo-
sure. This suggests that the risk of breast cancer is preventable if we eat
foods that will keep estrogen levels under control. The sad truth is that
most women simply are not aware of this evidence. If this information
were properly reported by responsible and credible public health agen-
cies, I suspect that many more young women might be taking very real,
very effective steps to avoid this awful disease.

THE COMMON ISSUES

Genes

Understandably women who are most afraid of this disease have a fam-
ily history of breast cancer. Family history implies that genes do play a
role in the development of breast cancer. But I hear too many people say
in effect, that "it's all in the family" and deny that they can do anything
to help themselves. This fatalistic attitude removes a sense of personal
responsibility for one's own health and profoundly limits available op-
tions.

It is true that if you have a family history of breast cancer, you are at
an increased risk of getting the disease. 23,24 However, one research group
found that less than 3% of all breast cancer cases can be attributed to
family history. 24 Even though other groups have estimated that a higher
percentage of cases are due to family history, 25 the vast majority of breast

162

THE CHINA STUDY

cancer in American women is not due to family history or genes. But
genetic fatalism continues to define the nation's mindset.

Among the genes that influence breast cancer risk, BRCA-1 and
BRCA-2 have received the most attention since their discovery in
1994. 26-29 These genes, when mutated, confer a higher risk both for
breast and ovarian cancers. 30, 31 These mutated genes may be passed on
from generation to generation; that is, they are inherited genes.

In the excitement over these discoveries, however, other information
has been ignored. First, only 0.2% of individuals in the general popu-
lation (1 in 500) carry the mutated forms of these genes. 25 Because of
the rarity of these genetic aberrations, only a few percent of the breast
cancer cases in the general population can be attributed to mutated
BRCA-1 or BRCA-2 genes. 32, 33 Second, these genes are not the only
genes that participate in the development of this disease 32 ; many more
will surely be discovered. Third, the mere presence of BRCA-1, BRCA-2
or any other breast cancer gene does not guarantee disease occurrence.
Environmental and dietary factors play a central role in determining
whether these genes are expressed.

A recent paper 31 reviewed twenty-two studies that assessed the risk
of breast (and ovarian) cancer among women who carried mutated
BRCA-1 and BRCA-2 genes. Overall, disease risk was 65% for breast
cancer and 39% for ovarian cancer by age seventy for BRCA-1 women,
and 45% and 11%, respectively, for BRCA-2 women. Women with these
genes certainly face high risks for breast cancer. But even among these
high-risk women, there is still good reason to believe that more atten-
tion to diet is likely to pay handsome rewards. About half of the women
who carry these rare, potent genes do not get breast cancer.

In short, although the discovery of BRCA-1 and BRCA-2 added an
important dimension to the breast cancer story, the excessive emphasis
given to these particular genes and genetic causation in general is not
warranted.

I do not mean to diminish the importance of knowing all there is to
know about these genes for the small minority of women who carry
them. But we need to remind ourselves that these genes need to be
"expressed" in order for them to participate in disease formation, and
nutrition can affect this. We've already seen in chapter three how a diet
high in animal-based protein has the potential to control genetic expres-
sion.

COMMON CANCERS: BREAST, PROSTATE, LARGE BOWEL

163

Screening and Non-Nutritional Prevention

With all of this new information regarding genetic risk and family his-
tory, women are often encouraged to get screened for breast cancer.
Screening is a reasonable step, especially for women who may have
tested positive for the BRCA genes. But it's important to remember that
doing a mammography or getting a genetic test to see if you harbor
BRCA genes does not constitute prevention of breast cancer.

Screening is merely an observation to see whether the disease has
progressed to an observable state. Some studies 34-36 have found that
groups of women who undergo frequent mammography have slightly
lower mortality rates than groups of women who do not undergo fre-
quent mammography. This implies that our cancer treatments are more
likely to be successful if the cancer is found at an earlier stage. This is
likely to be true, but there is some concern over the way statistics are
used in this debate.

One of the statistics used to support early detection and the ensuing
treatments is that once diagnosed with breast cancer, the likelihood of
surviving for at least five years is higher than ever before. 37 What this
really means is that with the aggressive campaign for regular screening,
many women are discovering their breast cancer at an earlier stage of
disease. When disease is discovered at an earlier stage it is less likely to
lead to death within five years, regardless of treatment. As a consequence,
we may have an improved five-year survival rate simply because women
find out that they have breast cancer earlier in the disease progression, not
because our treatments have improved over time. 38

Beyond the current screening methods, there are other non-nutri-
tional options for prevention that have been promoted. They are espe-
cially of interest to women who have a high risk of breast cancer due to
family history and/or to the presence of the BRCA genes. These options
include taking a drug such as tamoxifen and/or mastectomy.

Tamoxifen is one of the most popular drugs taken to prevent breast
cancer, 39 ' 40 but the long-term benefits of this option are not clear. One
major U.S. study showed that tamoxifen administered over a period of
four years to women at increased risk of breast cancer reduced the num-
ber of cases by an impressive 49%. 41 This benefit, however, may be limited
to women whose estrogen levels are very high. It was this result that led
the U.S. Food and Drug Administration to approve use of tamoxifen by
women who met certain criteria. 42 Other studies suggest that the enthusi-

164

THE CHINA STUDY

asm for this drug is not warranted. Two less substantial European trials 43 '
44 have failed to show any statistically significant tamoxifen benefit, rais-
ing some doubt about how dramatic the benefit really is. Moreover, there
is the additional concern that tamoxifen raises the risks for stroke, uter-
ine cancer, cataracts, deep vein thrombosis and pulmonary embolism,
although the overall benefits of breast cancer prevention are still believed
to outweigh the risks. 42 Other chemicals have also been investigated as
alternatives to tamoxifen, but these drugs are encumbered by limited ef-
fectiveness and/or some of the same troublesome side effects. 45 ' 46

Drugs such as tamoxifen and its newer analogues are considered anti-
estrogen drugs. In effect, they work by reducing the activity of estrogen,
which is known to be associated with elevated breast cancer risk. 4 - 5 My
question is quite simple: why don't we ask why estrogen is so high in
the first place, and once we recognize its nutritional origin, why don't
we then correct that cause? We now have enough information to show
that a diet low in animal-based protein, low in fat and high in whole
plant foods will reduce estrogen levels. Instead of suggesting dietary
change as a solution, we spend hundreds of millions of dollars develop-
ing and publicizing a drug that may or may not work and that almost
certainly will have unintended side effects.

The ability of dietary factors to control female hormone levels has
long been known in the research community, but a recent study was
particularly impressive. 47 Several female hormones, which increase
with the onset of puberty, were lowered by 20-30% (even 50% lower
levels for progesterone!) simply by having girls eight to ten years of
age consume a modestly low-fat, low animal-based food diet for seven
years. 47 These results are extraordinary because they were obtained with
a modest dietary change and were produced during a critical time of a
young girl's life, when the first seeds of breast cancer were being sowed.
These girls consumed a diet of no more than 28% fat and less than 150
nig cholesterol/day: a moderate plant-based diet. I believe that had they
consumed a diet devoid of animal-based foods and had they started this
diet earlier in life, they would have seen even greater benefits, including
a delay in puberty and an even lower risk of breast cancer later in life.

Women at high risk for breast cancer are given three options: watch
and wait, take tamoxifen medication for the remainder of their lives or
undergo mastectomy. There should be a fourth option: consuming a
diet free of animal-based foods and low in refined carbohydrates, aided
by regular monitoring for those at high risk. I stand by the usefulness

COMMON CANCERS: BREAST, PROSTATE, LARGE BOWEL

165

of this fourth option even for women who have already had a first mas-
tectomy. Using diet as an effective treatment of already-diagnosed dis-
ease has been well documented in human studies with advanced heart
disease, 48 ' 49 clinically documented Type 2 diabetes (see chapter seven),
advanced melanoma 50 (a deadly skin cancer) and, in experimental ani-
mal studies, 51 liver cancer.

Environmental Chemicals

There is another breast cancer conversation that has been taking place
for some years now. It concerns environmental chemicals. These widely
distributed chemicals have been shown to disrupt hormones, although
it is not clear which hormones in humans are being disrupted. These
chemicals may also cause reproductive abnormalities, birth defects and
Type 2 diabetes.

There are many different types of offending chemicals, most of which
are commonly associated with industrial pollution. One group, includ-
ing dioxins and PCBs, persist in the environment because they are not
metabolized when consumed. Thus they are not excreted from the body.
Because of this lack of metabolism, these chemicals accumulate in body
fat and breast milk of lactating mothers. Some of these chemicals are
known to promote the growth of cancer cells, although humans may
not be at significant risk unless one consumes excessive quantities of
meat, milk and fish. Indeed, 90-95% of our exposure to these chemicals
comes from consuming animal products — yet another reason why con-
suming animal-based foods can be risky.

There is a second group of these environmental chemicals that are also
commonly perceived to be significant causes of breast 52 and other can-
cers. They are called PAHs (Polycyclic Aromatic Hydrocarbons) and are
found in auto exhaust, factory smoke stacks, petroleum tar products and
tobacco smoke, among other processes common to an industrial society
Unlike the PCBs and dioxins, when we consume PAHs (in food and wa-
ter), we can metabolize and excrete them. But there is a snag: when the
PAHs are metabolized within the body, they produce intermediate prod-
ucts that react with DNA to form tightly bound complexes, or adducts
(see chapter three). This is the first step in causing cancer. In fact, these
chemicals have recently been shown to adversely affect the BRCA-1 and
BRCA-2 genes of breast cancer cells grown in the laboratory. 53

In chapter three, I described studies in my laboratory showing that
when a very potent carcinogen is put into the body, the rate at which

166

THE CHINA STUDY

it causes problems is mostly controlled by nutrition. Thus the rate at
which PAHs are metabolized into products that bind to DNA is very
much controlled by what we eat. Very simply, consuming a Western-
type diet will increase the rate at which chemical carcinogens like PAHs
bind to DNA to form products that cause cancer.

So when a recent study found slightly increased levels of PAH-DNA
adducts in women with breast cancer in Long Island, New York, 54 it
may well have been that these women were consuming a more meaty
diet, which increased the binding of the PAHs to DNA. It is entirely pos-
sible that the quantity of PAHs being consumed had nothing to do with
increasing breast cancer risk. In fact, in this study, the number of PAH-
DNA adducts in these women seem to be unrelated to PAH exposure. 54
How is this possible? Perhaps all of the women in this Long Island study
consumed a relatively uniform, low level of PAHs, and the only ones
who subsequently got breast cancer were the ones who ate a diet high
in fat and animal protein, thus causing more of the ingested PAHs to
bind to their DNA.

In this same Long Island study, breast cancer was not associated
with PCBs and dioxins, the chemicals that can't be metabolized. 55 As
a result of the Long Island study, the hype associating environmental
chemicals with breast cancer has been somewhat muted. This and
other findings suggest that environmental chemicals seem to play a
far less significant role for breast cancer than the kind of foods we
choose to eat.

Hormone Replacement Therapy

I must briefly mention one final breast cancer issue: whether to use hor-
mone replacement therapy (HRT), which increases breast cancer risk.
HRT is taken by many women in order to alleviate unpleasant effects of
menopause, protect bone health and prevent coronary heart disease. 56
However, it is now becoming widely acknowledged that HRT is not as
beneficial as once thought, and it may have certain severe side effects.
So what are the facts?

I am writing this commentary at an opportune time because the
results of some large trials of HRT use have been released in the last
year. 56 Of special interest are two large randomized intervention trials:
the Women's Health Initiative (WHI) 57 and the Heart and Estrogen/
Progestin Replacement Study (HERS). 58 Among women who take HRT,
after 5.2 years the WHI trial is showing a 26% increase in breast cancer

COMMON CANCERS: BREAST, PROSTATE, LARGE BOWEL

167

cases while the HERS study is seeing an even greater 30% increase. 59
These studies are consistent. It appears that increased exposure to fe-
male hormones, via HRT, does indeed lead to more breast cancer.

It has been thought that HRT is associated with lower rates of coro-
nary heart disease. 36 However, this is not necessarily true. In the large
WHI trial, for every 10,000 healthy postmenopausal women who took
HRT, there were seven more women with heart disease, eight more with
strokes and eight more with pulmonary embolism 37 — the opposite of
what had been expected. HRT may increase cardiovascular disease risk
after all. On the other hand, HRT did have a beneficial effect on colorec-
tal cancer and bone fracture rate. Among every 10,000 women, there
were six fewer colorectal cancers and five fewer bone fractures. 37

So how do you make a decision with such information? Just by add-
ing and subtracting the numbers we can see that HRT may well be the
cause of more harm than good. We can tell each individual woman to
make her own decision depending on which disease and which un-
pleasantry she fears the most, as many physicians are likely to do. But
this can be a tough decision for women who are having a difficult time
with menopause. These women must choose between living unaided
through the emotional and physical symptoms of menopause in order
to preserve a low risk of breast cancer, or taking HRT to manage their
menopause discomforts while increasing their risk of breast cancer and,
possibly cardiovascular disease. To say that this scenario troubles me
would be an understatement. We have spent well over a billion dollars
on the research and development of these HRT medical preparations,
and all we get is some apparent pluses and probably even more minuses.
Calling this troubling doesn't begin to describe it.

Instead of relying on HRT, 1 suggest that there is a better way, using
food. The argument goes like this:

• During the reproductive years, hormone levels are elevated, al-
though the levels among women who eat plant-based diets are not
as elevated.

• When women reach the end of their reproductive years, it is en-
tirely natural for reproductive hormones of all women to drop to a
low "base" level.

• As reproductive years come to an end, the lower hormone levels
among plant eaters don't crash as hard as they do among animal
eaters. Using hypothetical numbers to illustrate the concept, the

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THE CHINA STUDY

levels of plant eaters may crash from forty to fifteen, rather than
sixty to fifteen for animal eaters.

• These abrupt hormone changes in the body are what cause meno-
pausal symptoms.

• Therefore, a plant-based diet leads to less severe hormone crash
and a gentler menopause.

This argument is eminently reasonable based on what we know, al-
though more studies would be helpful. But even if future studies fail to
confirm these details, a plant-based diet still offers the lowest risk for
both breast cancer and heart disease for other reasons. It might just be
the best of all worlds, something that no drug can offer.

In each of the various issues involving breast cancer risk (tamoxifen
use, HRT use, environmental chemical exposure, preventive mastec-
tomy), I am convinced that these practices are distractions that prevent
us from considering a safer and far more useful nutritional strategy. It is
critical that we change the way we think about this disease, and that we
provide this information to the women who need it.

LARGE BOWEL CANCER
(INCLUDING COLON AND RECTUM)

At the end of June 2002, George W. Bush handed the presidency over to
Dick Cheney for a period of roughly two hours while he underwent a
colonoscopy. Because of the implications President Bush's colonoscopy
had for world politics, the story made national news, and colon and rec-
tal screening were briefly thrust into the spotlight. Across the country,
whether the comedians were making jokes or the news anchors were
describing the drama, everybody was suddenly, briefly, talking about
this thing called a colonoscopy and what it was for. It was a rare mo-
ment in which the country turned its focus to some of the most prolific
killer diseases, colon and rectal cancers.

Because colon and rectal cancers are both cancers of the large bowel,
and because of their other similarities, they often are grouped together
under the term colorectal cancer. Colorectal cancer is the fourth most
common cancer worldwide, in terms of overall mortality. 60 It is the sec-
ond most common in the United States, with 6% of Americans getting the
cancer during their lifetime. 37 Some even claim that, by age seventy, one-
half of the population of "Westernized" countries will develop a tumor in
the large bowel and 10% of these cases will progress to a malignancy. 61

COMMON CANCERS: BREAST, PROSTATE, LARGE BOWEL

169

GEOGRAPHIC DISPARITY

North America, Europe, Australia and wealthier Asian countries (Ja-
pan, Singapore) have very high rates of colorectal cancer, while Africa,
Asia and most of Central and South America have very low rates of this
cancer. For example, the Czech Republic has a death rate of 34.19 per
100,000 males, while Bangladesh has a death rate of 0.63 per 100,000
males! 62 63 Chart 8.3 shows a comparison of average death rates between
more developed countries and less developed countries; all these rates
are age-adjusted.

The fact that rates of colorectal cancer vary hugely between countries
has been known for decades. The question has always been why. Are the
differences due to genetics, or to environment?

It seems that environmental factors, including diet, play the most
important roles in colorectal cancer. Migrant studies have shown that
as people move from a low-cancer risk area to a high-cancer risk area,
they assume an increased risk within two generations. 64 This suggests
that diet and lifestyle are important causes of this cancer. Other stud-
ies have also found that rates of colorectal cancer change rapidly as a
population's diet or lifestyle changes. 64 These rapid changes in cancer
rates within one population cannot possibly be explained by changes in
inherited genes. In the context of human society, it takes thousands of

CHART 8.3: COLORECTAL CANCER DEATH RATE IN "MORE
DEVELOPED" COUNTRIES AND "LESS DEVELOPED" COUNTRIES

Death

16-

Rate per
100,000
People
(age-
adjusted)

14-

12 -

10-

■ Male

□ Female

More
Developed
Countries

Less
Developed
Countries

170

THE CHINA STUDY

years to get widespread, permanent changes in the inherited genes that
are passed from one generation to the next. Clearly, something about
environment or lifestyle is either preventing or enhancing the risk of
getting colorectal cancer.

In a landmark paper published almost thirty years ago, researchers
compared environmental factors and cancer rates in thirty-two coun-
tries around the world. 65 One of the strongest links between any cancer
and any dietary factor was between colon cancer and meat intake. Chart
8.4 shows this link for women in twenty-three different countries.

In this report, countries where more meat, more animal protein, more
sugar and fewer cereal grains were consumed had far higher rates of
colon cancer. 65 Another researcher whom I mentioned in chapter four,
Denis Burkitt, hypothesized that intake of dietary fiber was essential for
digestive health in general. He compared stool samples and fiber intakes
in Africa and Europe and proposed that colorectal cancers were largely
the result of low fiber intake. 66 Fiber, remember, is only found in plant
foods. It is the part of the plant that our body cannot digest. Using data
from another famous study that compared diets in seven different coun-
tries, researchers found that eating an additional ten grams of dietary
fiber a day lowered the long-term risk of colon cancer by 33%. 67 There
are ten grams of fiber in one cup of red raspberries, one Asian pear or

CHART 8.4: FEMALE COLON CANCER INCIDENCE
AND DAILY MEAT CONSUMPTION

50 -i

30 -

10 -

NEW ZEALAND.

• U.S.A.

• CANADA

DENMARK

JAMAICA
YUGOSLAVIA*

NORWAY

SWEDEN

•_ NETHERLANDS

• UK

• ISRAEL

„FDR

• ICELAND

JAPAN*
^NIGERIA

1 —

CHILE

FINLAND PUERTO RICO GERMANY
• « POLAND

ROMANIA •HUNGARY

' •COLOMBIA

120

160

200

240

280

320

Per Capita Daily Meat Consumption (grams)

COMMON CANCERS: BREAST, PROSTATE, LARGE BOWEL

171

one cup of peas. A cup of just about any variety of bean would provide
significantly more than ten grams of fiber.

From all this research, it seems clear that something can be said for
the importance of diet in colorectal cancer. But what exactly stops colon
and rectal cancer? Is it fiber? Is it fruits and vegetables? Is it carbohy-
drates? Is it milk? Each of these foods or nutrients has been suggested to
play a role. The debate has raged, and solid answers are seldom agreed
upon.

THE SPECIFIC CURE

Most of the debate over the past twenty-five years on dietary fiber and
its link to large bowel cancer began with Burkitt's work in Africa. Be-
cause of Burkitt's prominence, many people have believed that fiber is
the source of colorectal health. Perhaps you have already heard that
fiber is good for preventing colon cancer. At least you probably have
heard that fiber "keeps things running well." Isn't that what prunes are
known for?

Yet nobody has ever been able to prove that fiber is the magic bullet
for preventing colorectal cancer. There are important technical reasons
why a definitive conclusion regarding fiber is difficult to make. 68 Each
of these reasons is related either directly or indirectly to the fact that
dietary fiber is not a single, simple substance producing a single, simple
benefit. Fiber represents hundreds of substances, and "its" benefits
operate through an exceptionally complex series of biochemical and
physiological events. Each time researchers assess the consumption
of dietary fiber, they must decide which of the hundreds of fiber sub-
fractions to measure and which methods to use. It is nearly impossible
to establish a standard procedure because it is virtually impossible to
know what each fiber sub-fraction does in the body.

The uncertainty of having a standard procedure prompted us to
measure fiber in more than a dozen ways in our China Study. As sum-
marized in chapter four, as consumption of almost all of these fiber
types went up, colon and rectal cancer rates went down. 69 But we could
make no clear interpretations 70 as to which type of fiber was especially
important.

Despite the uncertainties, I continue to believe that Burkitt's 66 ini-
tial hypothesis that fiber-containing diets prevent colorectal cancers is
correct and that some of this effect is due to the aggregate effect of all
the fiber types. In fact, the hypothesis that dietary fiber prevents large

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THE CHINA STUDY

bowel cancers has become even more convincing. In 1990, a group of
researchers reviewed sixty different studies that had been done on fiber
and colon cancer. 71 They found that most of the studies supported the
idea that fiber protects against colon cancer. They noted that the com-
bined results showed that the people who consumed the most fiber had
a 43% lower risk of colon cancer than the people who consumed the
least fiber. 71 Those who consume the most vegetables had a 52% lower
risk than those who consume the least vegetables. 71 But even in this
large review of the evidence, researchers noted, "the data do not permit
discrimination between effects due to fiber and non-fiber effects due to
vegetables." 71 So is fiber, all by itself, the magic bullet we've been look-
ing for? We still, in 1990, didn't know.

Two years later, in 1992, a different group of researchers reviewed
thirteen studies that had compared people with and without colorectal
cancer (case-control design). 72 They found that those who had con-
sumed the most fiber had a 47% lower risk of colorectal cancer than
those who consumed the least. 72 In fact, they found that if Americans
ate an additional thirteen grams of fiber a day from food sources (not as
supplements), about a third of all colorectal cancer cases in the U.S.
could be avoided. 72 If you'll remember, thirteen grams, in real world
terms, is the amount found in about a cup of any variety of beans.

More recently, a mammoth study called the EPIC study collected
data on fiber intake and colorectal cancer in 519,000 people across
Europe. 73 They found that the 20% of people who consumed the most
fiber in their diet, about thirty-four grams per day, had a 42% lower risk
of colorectal cancer than the 20% who consumed the least fiber in their
diet, about thirteen grams per day 73 It's important to note once again
that, as with all of these studies, dietary fiber was obtained in food, not
as supplements. So all we can say is "fiber-containing diets" seem to sig-
nificantly reduce the risk of colorectal cancer. We still can't say anything
definitive about isolated fiber itself. This means that attempts to add
isolated fiber to foods may not produce benefits. But consuming plant
foods naturally high in fiber is clearly beneficial. These foods include
vegetables (the non-root parts), fruits and whole grains.

In reality, we can't even be sure how much of the prevention of
colorectal cancer is due to fiber-containing foods, because as people
eat more of these foods they usually consume less animal-based foods.
In other words, are fruits, vegetables and whole grains protective, or is
meat dangerous? Or is it both? A recent study in South Africa helped

COMMON CANCERS: BREAST, PROSTATE, LARGE BOWEL

173

to answer these questions. White South Africans have seventeen times
more large bowel cancer than black South Africans, and this was first
thought to be due to the much higher consumption of dietary fiber
among black South Africans provided by unrefined maize. 74 However,
in more recent years, black South Africans have been increasingly con-
suming commercially refined maize-meal — maize minus its fiber. They
now eat even less fiber than the white South Africans. Yet, colon cancer
rates among blacks remain at a low level, 75 which calls into question
how much of the cancer-protective effect is due to dietary fiber alone.
A more recent study 76 showed that the higher colon cancer rates among
white South Africans could well be due to their elevated consumption
of animal protein (77 vs. 25 g/day), total fat (115 vs. 71 g/day) and
cholesterol (408 vs. 211 mg/day), as seen in Chart 8.5. The researchers
suggested that the much higher colon cancer rates among white South

CHART 8.5: INTAKE OF ANIMAL PROTEIN, TOTAL FAT AND
CHOLESTEROL AMONG BLACK AND WHITE SOUTH AFRICANS

Animal Protein Total Fat

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THE CHINA STUDY

Africans may be more related to the quantity of animal protein and fat in
their diets than their lacking the protective factor of dietary fiber. 76

What is clear is that diets naturally high in fiber and low in animal-
based foods can prevent colorectal cancer. Even in the absence of more
specific details, we can still make important public health recommenda-
tions. The data clearly show that a wholefoods, plant-based diet can dra-
matically lower colorectal cancer rates. We don't need to know which fiber
is responsible, what mechanism is involved or even how much of the effect
is independently due to fiber.

OTHER FACTORS

It has been recently noted that the same risk factors that promote
colorectal cancer, a diet low in fruits and vegetables and high in animal
foods and refined carbohydrates, can also promote insulin resistance
syndrome. 77-79 From there, scientists have hypothesized that insulin re-
sistance may be responsible for colon cancer. 77-82 Insulin resistance was
described in chapter six as a diabetic condition. And what's good for
keeping insulin resistance under control is also good for colon cancer: a
diet of whole, plant-based foods.

This diet happens to be very high in carbohydrates, which have
recently been under assault in the marketplace. Because carbohydrate-
confusion persists, let me remind you that there are two different types
of carbohydrates: refined carbohydrates and complex carbohydrates.
Refined carbohydrates are the starches and sugars obtained from plants
by mechanically stripping off their outer layers, which contain most of
the plant's vitamins, minerals, protein and fiber. This "food" (regular
sugar, white flour, etc.) has very little nutritional value. Foods such as
pastas made from refined flour, sugary cereals, white bread, candies and
sugar-laden soft drinks should be avoided as much as possible. But do
eat whole, complex carbohydrate-containing foods such as unprocessed
fresh fruits and vegetables, and whole grain products like brown rice
and oatmeal. These unprocessed carbohydrates, especially from fruits
and vegetables, are exceptionally health-promoting.

You also may have heard that calcium is beneficial in fighting colon
cancer. This, of course, gets extended to the argument that cow's milk
fights colon cancer. It has been hypothesized that high-calcium diets
prevent colon cancer in two ways: first, it inhibits the growth of critical
cells in the colon, 83 84 and second, it binds up intestinal bile acids. These
bile acids arise in the liver, move to the intestine and are thought to get

COMMON CANCERS: B R EAST, PROSTATE, LARGE BOWEL

175

into the large bowel and promote colon cancer development. By binding
these bile acids, calcium is said to prevent colon cancer.

One research group demonstrated that high-calcium diets — generally
meaning diets high in dairy foods — inhibit the growth of certain cells in
the colon, 84 but this effect was not entirely consistent for the various indica-
tors of cell growth. Furthermore, it is not clear whether these presumably
favorable biochemical effects really lead to less cancer growth. 83 ' 85 Another
research group demonstrated that calcium does reduce the presum-
ably dangerous bile acids, but also observed that a high-wheat diet did
an even better job of reducing the bile acids. 66 But — and this is the really
odd part — when a combination high-calcium and high-wheat diet was
consumed, the binding effect on bile acids was weaker than for each
individual supplement taken alone. 86 It just goes to show that when
individually-observed nutrient effects are combined, as in a dietary situ-
ation, the expected may become the unexpected.

I doubt that a high-calcium diet, obtained through calcium supple-
ments or through calcium-rich cow's milk, has a beneficial effect on
colon cancer. In rural China where calcium consumption is modest and
almost no dairy food is consumed, 87 colon cancer rates are not higher;
instead they are much lower than in the U.S. The parts of the world that
consume the most calcium, Europe and North America, have the high-
est rates of colorectal cancer.

Another lifestyle choice that is clearly important for this disease is
exercise. Increased exercise is convincingly associated with less colorec-
tal cancer. In one summary from the World Cancer Research Fund and
the American Institute for Cancer Research, seventeen out of twenty
studies found that exercise protected against colon cancer. 64 Unfortu-
nately, there seems to be no convincing evidence as to why or how this
occurs.

SCREENING FOR TROUBLE

The benefits of exercise bring me back to President George W. Bush. He
is known to enjoy staying physically fit with a regular running routine,
and that is undoubtedly one of the reasons why he received a clean bill
of health when he had a colonoscopy. But what is a colonoscopy anyway
and is it really worth the effort to get checked? When people go to the
doctor to get a colonoscopy, the doctor inspects the large bowel using a
rectal probe and looks for abnormal tissue growth. The most commonly
found abnormality is a polyp. Although it is not yet clear exactly how tu-

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THE CHINA STUDY

mors are related to polyps, most scientists would agree 88,89 that they share
similar dietary associations and genetic characteristics. Those people who
have noncancerous problems in the large bowel, such as polyps, often are
the same people who later develop cancerous tumors.

So getting screened for polyps or other problems is a reasonable
way to establish risk for large bowel cancer in the future. But what if
you have a polyp? What is the best thing to do? Will surgical removal
of the polyp lessen colon cancer risk? A nationwide study has shown
that, when polyps were removed, there was a 76-90% decrease in the
expected cases of colon cancer. 89, 90 This certainly supports the idea of
routine screening. 89, 91 It is commonly recommended that people get a
colonoscopy once every ten years starting at the age of fifty. If you have
a higher risk of colorectal cancer, it is recommended that you start at the
age of forty and screen more frequently.

How do you know if you are at a higher risk for colorectal cancer? We
can very roughly assess our personal genetic risk in several ways. We
can consider the probability of our getting colon cancer based on the
number of immediate family members who already have the disease, we
can screen for the presence of polyps, and we now can clinically test for
the presence of suspect genes. 92

This is an excellent example of how genetic research can lead to a bet-
ter understanding of complex diseases. However, in the enthusiasm for
studying the genetic basis for this cancer, two things often get overlooked.
First, the proportion of colon cancer cases attributed to known inherited
genes is only about 1-3%. 89 Another 10-30% 89 tend to occur in some
families more than others (called familial clustering), an effect possibly
reflective of a significant genetic contribution. These numbers, however,
exaggerate the number of cancers that are solely "due to genes."

Except for the very few people whose colon cancer risk is largely
determined by known inherited genes (1-3%), most of the family-con-
nected colon cancer cases (i.e, the additional 10-30%) are still largely
determined by environmental and dietary factors. After all, place of resi-
dence and diet are often shared experiences within families.

Even if you have a high genetic risk, a healthy plant-based diet is
capable of negating most, if not all, of that risk by controlling the ex-
pression of these genes. Because a high-fiber diet can only prevent colon
cancer — extra fiber won't ever promote colon cancer — dietary recom-
mendations should be the same regardless of one's genetic risk.

COMMON CANCERS: BREAST, PROSTATE, LARGE BOWEL

177

PROSTATE CANCER

I suspect that most people do not know exactly what a prostate is, even
though prostate cancer is commonly discussed. The prostate is a male
reproductive organ about the size of a walnut, located between the blad-
der and the colon. It is responsible for producing some of the fluid that
helps sperm on its quest to fertilize the female's egg.

For such a little thing, it sure can cause a lot of problems. Several of
my friends now have prostate cancer or closely related conditions, and
they aren't alone. As one recent report pointed out, "Prostate cancer is
one of the most commonly diagnosed cancers among men in the United

States, representing about 25% of all tumors " 93 As many as half of all

men seventy years and older have latent prostate cancer, 94 a silent form
of the cancer which is not yet causing discomfort. Prostate cancer is not
only extremely prevalent, but also slow-growing. Only 7% of diagnosed
prostate cancer victims die within five years. 95 This makes it difficult to
know how and if the cancer should be treated. The main question for
the patient and doctor is: will this cancer become life threatening before
death comes from other causes?

One of the markers used to determine the likelihood of prostate can-
cer becoming life threatening is the blood level of prostate specific anti-
gen (PSA). Men are diagnosed as having prostate problems when their
PSA levels are above four. But this test alone is hardly a firm diagnosis
of cancer, especially if the PSA level is barely above four. The ambiguity
of this test leads to some very difficult decision-making. Occasionally
my friends ask for my opinion. Should they have a little surgery or a lot?
Is a PSA value of 6.0 a serious problem or just a wake-up call? If it's a
wake-up call, then what must they do to reduce such a number? While
I cannot speak to the clinical condition of an individual, I can speak to
the research, and of the research I have seen, there is no doubt that diet
plays a key role in this disease.

Although there is debate regarding the specifics of diet and this can-
cer, let's start with some very safe assumptions that have long been ac-
cepted in the research community:

• Prostate cancer rates vary widely between different countries, even
more than breast cancer.

• High prostate cancer rates primarily exist in societies with "West-
ern" diets and lifestyles.

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THE CHINA STUDY

• In developing countries, men who adopt Western eating practices
or move to Western countries suffer more prostate cancer.

These disease patterns are similar to those of other diseases of afflu-
ence. Mostly this tells us that although prostate cancer certainly has a
genetic component, environmental factors play the dominant role. So
what environmental factors are important? You can guess that I'm going
to say plant-based foods are good and animal-based foods are bad, but
do we know anything more specific? Surprisingly, one of the most con-
sistent, specific links between diet and prostate cancer has been dairy
consumption.

A 2001 Harvard review of the research could hardly be more convinc-
ing 96 :

. . . twelve of . . . fourteen case-control studies and seven of . . . nine
cohort studies [have] observed a positive association for some
measure of dairy products and prostate cancer; this is one of the
most consistent dietary predictors for prostate cancer in the published
literature [my emphasis]. In these studies, men with the highest
dairy intakes had approximately double the risk of total prostate
cancer, and up to a fourfold increase in risk of metastatic or fatal
prostate cancer relative to low consumers. 96

Let's consider that again: dairy intake is "one of the most consistent
dietary predictors for prostate cancer in the published literature," and
those who consume the most dairy have double to quadruple the risk.

Another review of published literature done in 1998 reached a simi-
lar conclusion:

In ecologic data, correlations exist between per capita meat and
dairy consumption and prostate cancer mortality rate [one study
cited]. In case control and prospective studies, the major con-
tributors of animal protein, meats, dairy products and eggs have
frequently been associated with a higher risk of prostate cancer . . .
[twenty-three studies cited]. Of note, numerous studies have
found an association primarily in older men [six studies cited]

though not all [one study cited] The consistent associations

with dairy products could result from, at least in part, their cal-
cium and phosphorous content. 97

COMMON CANCERS: BREAST, PROSTATE, LARGE BOWEL

179

In other words, an enormous body of evidence shows that animal-
based foods are associated with prostate cancer. In the case of dairy, the
high intake of calcium and phosphorus also could be partly responsible
for this effect.

This research leaves little room for dissent; each of the above stud-
ies represents analyses of over a dozen individual studies, providing an
impressive bulk of convincing literature.

THE MECHANISMS

As we have seen with other forms of cancer, large-scale observational
studies show a link between prostate cancer and an animal-based diet,
particularly one based heavily on dairy. Understanding the mechanisms
behind the observed link between prostate cancer and dairy clinches
the argument.

The first mechanism concerns a hormone that increases cancer
cell growth, a hormone that our bodies make, as needed. This growth
hormone, Insulin-like Growth Factor 1 (IGF-1), is turning out to be a
predictor of cancer just as cholesterol is a predictor for heart disease.
Under normal conditions, this hormone efficiently manages the rates at
which cells "grow" — that is, how they reproduce themselves and how
they discard old cells, all in the name of good health.

Under unhealthy conditions, however, IGF-1 becomes more active,
increasing the birth and growth of new cells while simultaneously in-
hibiting the removal of old cells, both of which favor the development
of cancer [seven studies cited 98 ] . So what does this have to do with the
food we eat? It turns out that consuming animal-based foods increases
the blood levels of this growth hormone, IGF-1. 99-101

With regard to prostate cancer, people with higher than normal blood
levels of IGF-I have been shown to have 5. 1 times the risk of advanced-
stage prostate cancer. 98 There's more: when men also have low blood
levels of a protein that binds and inactivates IGF-I, 102 they will have 9.5
times the risk oj advanced-stage prostate cancer, 98 Let's put a few stars by
these numbers. They are big and impressive — and fundamental to this
finding is the fact that we make more IGF-I when we consume animal-
based foods like meat and dairy. 99-101

The second mechanism relates to vitamin D metabolism. This "vi-
tamin" is not a nutrient that we need to consume. Our body can make
all that we need simply by being in sunlight fifteen to thirty minutes
every couple of days. In addition to the production of vitamin D being

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affected by sunlight, it is also affected by the food that we eat. The for-
mation of the most active form of vitamin D is a process that is closely
monitored and controlled by our bodies. This process is a great example
of our bodies' natural balancing act, affecting not only prostate cancer,
but breast cancer, colon cancer, osteoporosis and autoimmune diseases
like Type 1 diabetes. Because of its importance for multiple diseases,
and because of the complexity involved in explaining how it all works,
I have provided in Appendix C an abbreviated scheme, just enough to
illustrate my point. This web of reactions illustrates many similar and
highly integrated reaction networks showing how food controls health.

The main component of this process is an active form of vitamin D
produced in the body from the vitamin D that we get from food or sun-
shine. This active or "supercharged" D produces many benefits through-
out the body including the prevention of cancer, autoimmune diseases
and diseases like osteoporosis. This all-important supercharged D is not
something that you get from food or from a drug. A drug composed of
isolated supercharged D would be far too powerful and far too danger-
ous for medical use. Your body uses a carefully composed series of con-
trols and sensors to produce just the right amount of supercharged D for
each task at exactly the right time.

As it turns out, our diet can determine how much of this super-
charged D is produced and how it works once it is produced. Animal
protein that we consume has the tendency to block the production of
supercharged D, leaving the body with low levels of this vitamin D in
the blood. If these low levels persist, prostate cancer can result. Also,
persistently high intakes of calcium create an environment where super-
charged D declines, thus adding to the problem.

So what food substance has both animal protein and large amounts
of calcium? Milk and other dairy foods. This fits in perfectly with the
evidence that links dairy consumption with prostate cancer. This infor-
mation provides what we call biological plausibility and shows how the
observational data fit together. To review the mechanisms:

• Animal protein causes the body to produce more IGF-1, which in
turn throws cell growth and removal out of whack, stimulating
cancer development.

• Animal protein suppresses the production of "supercharged" D.

• Excessive calcium, as found in milk, also suppresses the produc-
tion of "supercharged" D.

COMMON CANCERS: BREAST, PROSTATE, LARGE BOWEL

181

• "Supercharged" D is responsible for creating a wide variety of
health benefits in the body. Persistently low levels of supercharged
D create an inviting environment for different cancers, autoim-
mune diseases, osteoporosis and other diseases.

The important story here is how the effects of food — both good and
bad — operate through a symphony of coordinated reactions to prevent
diseases like prostate cancer. In discovering the existence of these net-
works, we sometimes wonder which specific function comes first and
which comes next. We tend to think of these reactions within the net-
work as independent. But this surely misses the point. What impresses
me is the multitude of reactions working together in so many ways to
produce the same effect: in this case, to prevent disease.

There is no single "mechanism" that fully explains what causes dis-
eases such as cancer. Indeed, it would be foolish to even think along
these lines. But what I do know is this: the totality and breadth of the
evidence, operating through highly coordinated networks, supports the
conclusions that consuming dairy and meat are serious risk factors for
prostate cancer.

BRINGING IT TOGETHER

Roughly half a million Americans this year will go to the doctor's office
and be told that they have cancer of the breast, prostate or large bowel.
People who get one of these cancers represent 40% of all new cancer
patients. These three cancers devastate the lives of not only the victims
themselves, but also their family and friends.

When my mother-in-law died of colon cancer at the age of fifty-one,
none of us knew that much about nutrition or what it meant for health.
It wasn't that we didn't care about the health of our loved ones — of
course we did. We just didn't have the information. Yet, over thirty years
later, not much has changed. Of the people you know who have cancer,
or are at risk of having cancer, how many of them have considered the
possibility of adopting a whole foods, plant-based diet to improve their
chances? I'm guessing very few of them have done so. Probably they,
too, don't have the information.

Our institutions and information providers are failing us. Even cancer
organizations, at both the national and local level, are reluctant to discuss
or even believe this evidence. Food as a key to health represents a power-
ful challenge to conventional medicine, which is fundamentally built on

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drugs and surgery (see Part IV). The widespread communities of nutri-
tion professionals, researchers and doctors are, as a whole, either unaware
of this evidence or reluctant to share it. Because of these failings, Ameri-
cans are being cheated out of information that could save their lives.

There is enough evidence now that doctors should be discussing
the option of pursuing dietary change as a potential path to cancer
prevention and treatment. There is enough evidence now that the U.S.
government should be discussing the idea that the toxicity of our diet
is the single biggest cause of cancer. There is enough evidence now
that local breast cancer alliances, and prostate and colon cancer institu-
tions, should be discussing the possibility of providing information to
Americans everywhere on how a whole foods, plant-based diet may be
an incredibly effective anti-cancer medicine.

If these discussions were to happen, it is possible that, next year,
fewer than 500,000 people would go to the doctor's office and be told
they have cancer of the breast, prostate or large bowel. The year after
that, even fewer friends, coworkers and family members would be given
the most dreaded of all diagnoses. And the following year, even fewer.

The possibility that this future could be our reality is real, and as long
as this future holds such promise for the health of people everywhere, it
is a future worth working for.

Autoimmune Diseases

No group of diseases is more insidious than autoimmune diseases. They
are difficult to treat, and progressive loss of physical and mental func-
tion is a common outcome. Unlike heart disease, cancer, obesity and
Type 2 diabetes, with autoimmune diseases the body systematically at-
tacks itself. The afflicted patient is almost guaranteed to lose.

A quarter million people in the U.S. are diagnosed with one of the
forty separate autoimmune diseases each year. 1 ' 2 Women are 2.7 times
more likely to be afflicted than are men. About 3% of Americans (one in
every thirty-one people) have an autoimmune disease, a staggering total
of 8.5 million people; some people put the total at as many as 12-13
million people. 3

The more common of these diseases are listed in Chart 9.1. 2 The first
nine comprise 97% of all autoimmune disease cases. 2 The most studied
are multiple sclerosis (MS), rheumatoid arthritis, lupus, Type 1 diabetes
and rheumatic heart disease. 2 These are also the primary autoimmune
diseases that have been studied in reference to diet.

Others not listed in Chart 9.1 include inflammatory bowel disease, 4
Crohn's disease, 4 rheumatic heart disease 3 and (possibly) Parkinsons
disease. 5

Each disease name may sound very different, but as one recent re-
view points out, 2 "... it is important to consider . . . these disorders as
a group." They show similar clinical backgrounds , 3,6 ' 7 they sometimes
occur in the same person and they are often found in the same popula-
tions. 2 MS and Type 1 diabetes, for example, have "near(ly) identical

183

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CHART 9.1: COMMON AUTOIMMUNE DISEASES

(FROM MOST COMMON TO LEAST COMMON)

Graves' disease (Hyperthyroidism]

10. Sjogren's disease

Rheumatoid arthritis

1 1 . Myasthenia gravis

Thyroiditis (Hypothyroidism]

12. Polymyositis/dermatomyositis

Vitiligo

1 3. Addison's disease

Pernicious anemia

14. Scleroderma

Glomerulonephritis

1 5. Primary biliary cirrhosis

Multiple sclerosis

16. Uveitis

Type 1 diabetes

17. Chronic active hepatitis

Systemic lupus erythematosus

ethnic and geographic distribution." 8 Autoimmune diseases in general
become more common the greater the distance from the equator. This
phenomenon has been known since 1922. 9 MS, for example, is over a
hundred times more prevalent in the far north than at the equator. 10

Because of some of these common features, it is not too far-fetched
to think of the autoimmune diseases as one grand disease living in dif-
ferent places in the body and taking on different names. We refer in this
way to cancer, which is specifically named depending on what part of
the body it resides in.

All autoimmune diseases are the result of one group of mechanisms
gone awry, much like cancer. In this case, the mechanism is the immune
system mistakenly attacking cells in its own body. Whether it is the pan-
creas as in Type 1 diabetes, the myelin sheath as in MS or joint tissues
as in arthritis, all autoimmune diseases involve an immune system that
has revolted. It is an internal mutiny of the worst kind, one in which our
body becomes its own worst enemy.

IMMUNITY FROM INVADERS

The immune system is astonishingly complex. I often hear people
speaking about this system as if it were an identifiable organ like a lung.
Nothing could be further from the truth. It is a system, not an organ.

In essence, our immune system is like a military network designed to de-
fend against foreign invaders. The "soldiers" of this network are the white
blood cells, which are comprised of many different sub-groups, each having
its own mission. These sub-groups are analogous to a navy, army, air force
and marines, with each group of specialists doing highly specialized work.

AUTOIMMUNE DISEASES

185

The "recruitment center" for the system is in the marrow of our
bones. The marrow is responsible for generating specialized cells
called stem cells. Some of these cells are released into circulation for
use elsewhere in the body; these are called B-cells (for bone). Other
cells formed in the bone marrow remain immature, or unspecialized,
until they travel to the thymus (an organ in the chest cavity just above
the heart) where they become specialized; these are called T-cells (for
thymus). These "soldier" cells, along with other specialized cells, team
up to create intricate defense plans. They meet at major intersections
around the body including the spleen (just inside the left lower rib
cage) and the lymph nodes. These meeting points are like command
and control centers, where the "soldier cells" rearrange themselves into
teams to attack foreign invaders.

These cells are remarkably adaptable when they form their teams.
They are able to respond to different circumstances and different for-
eign substances, even those they have never before seen. The immune
response to these strangers is an incredibly creative process. It is one of
the true wonders of nature.

The foreign invaders are protein molecules called antigens. These
foreign cells can be a bacterium or a virus looking to corrupt the body's
integrity. So when our immune system notices these foreign cells, or
antigens, it destroys them. Each of these foreign antigens has a sepa-
rate identity, which is determined by the sequence of amino acids that
comprises its proteins. It is analogous to each and every person having
a different face. Because numerous amino acids are available for creating
proteins, there are infinite varieties of distinctive "faces."

To counter these antigens, our immune system must customize its
defense to each attack. It does this by creating a "mirror image" pro-
tein for each attacker. The mirror image is able to fit perfectly onto the
antigen and destroy it. Essentially, the immune system creates a mold
for each face it encounters. Every time it sees that face after the initial
encounter, it uses the custom-made mold to "capture" the invader and
destroy it. The mold may be a B-cell antibody or a T-cell-based receptor
protein.

Remembering each defense against each invader is what immuniza-
tion is all about. An initial exposure to chicken pox, for example, is a
difficult battle, but the second time you encounter that virus you will
know exactly how to deal with it, and the war will be shorter, less pain-
ful and much more successful. You may not even get sick.

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IMMUNITY FROM OURSELVES

Even though this system is a wonder of nature when it is defending the
body against foreign proteins, it is also capable of attacking the same
tissues that it is designed to protect. This self-destructive process is
common to all autoimmune diseases. It is as if the body were to commit
suicide.

One of the fundamental mechanisms for this self-destructive behav-
ior is called molecular mimicry. It so happens that some of the foreign
invaders that our soldier cells seek out to destroy look the same as our
own cells. The immune system "molds" that fit these invaders also fit
our own cells. The immune system then destroys, under some circum-
stances, everything that fits the mold, including our own cells. This is
an extremely complex self-destructive process involving many different
strategies on the part of the immune system, all of which share the same
fatal flaw of not being able to distinguish "foreign" invader proteins
from the proteins of our own body.

What does all of this have to do with what we eat? It so happens that
the antigens that trick our bodies into attacking our own cells may be
in food. During the process of digestion, for example, some proteins
slip into our bloodstream from the intestine without being fully broken
down into their amino acid parts. The remnants of undigested proteins
are treated as foreign invaders by our immune system, which sets about
making molds to destroy them and sets into motion the self-destructive
autoimmune process.

One of the foods that supply many of the foreign proteins that mimic
our own body proteins is cow's milk. Most of the time, our immune
system is quite smart. Just like an army arranges for safeguards against
friendly fire, the immune system has safeguards to stop itself from at-
tacking the body it's supposed to protect. Even though an invading
antigen looks just like one of the cells in our own body, the system can
still distinguish our own cells from the invading antigen. In fact, the im-
mune system may use our own cells to practice making molds against
the invader antigen without actually destroying the friendly cell.

This is analogous to training camps in preparations for war. When our
immune system is working properly, we can use the cells in our body that
look like the antigens as a training exercise, without destroying them, to
prepare our soldier cells to repulse the invading antigens. It is one more
example' of the exceptional elegance of nature's ability to regulate itself.

AUTOIMMUNE DISEASES

187

The immune system uses a very delicate process to decide which pro-
teins should be attacked and which should be left alone. 11 The way this
process, which is incredibly complex, breaks down with autoimmune
diseases is not yet understood. We just know that the immune system
loses its ability to differentiate between the body's cells and the invading
antigen, and instead of using the body's cells for "training," it destroys
them along with the invaders.

TYPE 1 DIABETES

In the case of Type 1 diabetes, the immune system attacks the pancreas
cells responsible for producing insulin. This devastating, incurable
disease strikes children, creating a painful and difficult experience for
young families. What most people don't know, though, is that there is
strong evidence that this disease is linked to diet and, more specifically
to dairy products. The ability of cow's milk protein to initiate Type 1
diabetes 12-14 is well documented. The possible initiation of this disease
goes like this:

• A baby is not nursed long enough and is fed cow's milk protein,
perhaps in an infant formula.

• The milk reaches the small intestine, where it is digested down to
its amino acid parts.

• For some infants, cow's milk is not fully digested, and small amino
acid chains or fragments of the original protein remain in the in-
testine.

• These incompletely digested protein fragments may be absorbed
into the blood.

• The immune system recognizes these fragments as foreign invad-
ers and goes about destroying them.

• Unfortunately, some of the fragments look exactly the same as the
cells of the pancreas that are responsible for making insulin.

• The immune system loses its ability to distinguish between the
cow's milk protein fragments and the pancreatic cells, and destroys
them both, thereby eliminating the child's ability to produce insu-
lin.

• The infant becomes a Type 1 diabetic, and remains so for the rest
of his or her life.

This process boils down to a truly remarkable statement: cow's milk
may cause one of the most devastating diseases that can befall a child. For

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obvious reasons, this is one of the most contentious issues in nutrition
today.

One of the more remarkable reports on this cow's milk effect was
published over a decade ago, in 1992, in the New England Journal oj
Medicine. 12 The researchers, from Finland, obtained blood from Type
1 diabetic children, aged four to twelve years. Then they measured the
levels of antibodies that had formed in the blood against an incomplete-
ly digested protein of cow's milk called bovine serum albumin (BSA).
They did the same process with non-diabetic children and compared
the two groups (remember, an antibody is the mirror image, or "mold,"
of a foreign antigen). Children who had antibodies to cow's milk protein
must have previously consumed cow's milk. It also means that undi-
gested protein fragments of the cow's milk proteins had to have entered
the infant's circulation in order to cause the formation of antibodies in
the first place.

The researchers discovered something truly remarkable. Of the 142
diabetic children measured, every single one had antibody levels higher
than 3.55. Of the seventy-nine normal children measured, every single
one had antibody levels less than 3.55.

There is absolutely no overlap between antibodies of healthy and
diabetic children. All of the diabetic children had levels of cow's milk
antibodies that were higher than those of all of the non-diabetic chil-
dren. This implies two things: children with more antibodies consumed
more cow's milk, and second, increased antibodies may cause Type 1
diabetes.

These results sent shock waves through the research community It
was the complete separation of antibody responses that made this study
so remarkable. This study, 12 and others even earlier, 15-17 initiated an ava-
lanche of additional studies over the next several years that continue to
this day. 13 - 18 - 19

Several studies have since investigated this effect of cow's milk on
BSA antibody levels. All but one showed that cow's milk increases BSA
antibodies in Type 1 diabetic children, 18 although the responses were
quite variable in their magnitude.

Over the past decade, scientists have investigated far more than
just the BSA antibodies, and a more complete picture is coming into
view. Very briefly, it goes something like this 13, 19 : infants or very young
children of a certain genetic background, 20, 21 who are weaned from the
breast too early 22 onto cow's milk and who, perhaps, become infected

AUTOIMMUNE DISEASES

189

with a virus that may corrupt the gut immune system, 19 are likely to
have a high risk for Type 1 diabetes. A study in Chile 23 considered the
first two factors, cow's milk and genes. Genetically susceptible children
weaned too early onto cow's milk-based formula had a risk of Type 1 di-
abetes that was 13.1 times greater than children who did not have these
genes and who were breast-fed for at least three months (thus minimiz-
ing their exposure to cow's milk). Another study in the U.S. showed that
genetically susceptible children fed cow's milk as infants had a risk of
disease that was 1 1.3 times greater than children who did not have these
genes and who were breast-fed for at least three months. 24 This eleven
to thirteen times greater risk is incredibly large (1,000-1,200%!); any-
thing over three to four times is usually considered very important. To
put this in perspective, smokers have approximately ten times greater
risk of getting lung cancer (still less than the eleven to thirteen times
risk here) and people with high blood pressure and cholesterol have a
2.5-3.0 times greater risk of heart disease (Chart 9.2). 18

So how much of the eleven to thirteen times increased risk of Type
1 diabetes is due to early exposure to cow's milk, and how much is due

CHART 9.2: RELATIVE RISKS OF VARIOUS FACTORS
ON VARIOUS DISEASE OUTCOMES

1,200%
1,000%-
800% ■

£=

> 600%

£ 400% -

200%

Heart

Disease

High Blood Pressure Smoking
and Cholesterol

Cow's Milk
+ High-Risk Genes

Risk Factors

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to genes? These days, there is a popular opinion that Type 1 diabetes is
due to genetics, an opinion often shared by doctors as well. But genetics
alone cannot account for more than a very small fraction of cases of this
disease. Genes do not act in isolation; they need a trigger for their ef-
fects to be produced. It has also been observed that after one member of
identical twin pairs gets Type 1 diabetes, there is only a 13-33% chance
of the second twin getting the disease, even though both twins have
the same genes. 13, 20, 21 • 25 - 16 If it were all due to genes, closer to 100% of
the identical twins would get the disease. In addition, it is possible that
the 13-33% risk for the second twin is due to the sharing of a common
environment and diet, factors affecting both twins.

Consider, for example, the observation shown in Chart 9.3, which
highlights the link between one aspect of environment, cow's milk con-
sumption, and this disease. Cow's milk consumption by children zero
to fourteen years of age in twelve countries 27 shows an almost perfect
correlation with Type 1 diabetes. 28 The greater the consumption of
cow's milk, the greater the prevalence of Type 1 diabetes. In Finland,
Type 1 diabetes is thirty-six times more common than in Japan. 29 Large
amounts of cow's milk products are consumed in Finland but very little
is consumed in Japan. 27

CHART 9.3: ASSOCIATION OF COW'S MILK CONSUMPTION AND
INCIDENCE OF TYPE 1 DIABETES IN DIFFERENT COUNTRIES

0 100 200 300

Cow Milk Consumption (liters/person/year)

AUTOIMMUNE DISEASES

191

As we have seen with other diseases of affluence, when people migrate
from areas of the world where disease incidence is low to areas of the
world where disease incidence is high, they quickly adopt the high inci-
dence rates as they change their diet and lifestyle. 30 " 32 This shows that even
though individuals may have the necessary gene(s), the disease will occur
only in response to certain dietary and/or environmental circumstances.

Disease trends over time show the same thing. The worldwide preva-
lence of Type 1 diabetes is increasing at an alarming rate of 3% per year. 33
This increase is occurring for different populations even though there
may be substantial differences in disease rates. This relatively rapid in-
crease cannot be due to genetic susceptibility The frequency of any one
gene in a large population is relatively stable over time, unless there are
changing environmental pressures that allow one group to reproduce
more successfully than another group. For example, if all families with
Type 1 diabetic relatives had a dozen babies and all the families without
Type 1 diabetic relatives died off, then the gene or genes that may be
responsible for Type 1 diabetes would become much more common in
the population. This, of course, is not what is happening, and the fact
that Type 1 diabetes is increasing 3% every year is very strong evidence
that genes are not solely responsible for this disease.

It seems to me that we now have impressive evidence showing that
cow's milk is likely to be an important cause of Type 1 diabetes. When
the results of all these studies are combined (both genetically suscep-
tible and not susceptible), we find that children weaned too early and
fed cow's milk have, on average, a 50-60% higher risk of Type 1 diabetes
(1.5-1.6 times increased risk). 34

The earlier information on diet and Type 1 diabetes was impressive
enough to cause two significant developments. The American Academy
of Pediatrics in 1994 "strongly encouraged" that infants in families
where diabetes is more common not be fed cow's milk supplements for
their first two years of life. Second, many researchers 19 have developed
prospective studies — the kind that follow individuals into the future —
to see if a careful monitoring of diet and lifestyle could explain the onset
of Type 1 diabetes.

Two of the better known of these studies have been underway in Fin-
land, one starting in the late 1980s 13 and the other in the mid-1990s. 35
One has shown that cow's milk consumption increases the risk of Type
1 diabetes five- to sixfold, 36 while the second 35 tells us that cow's milk
increases the development of at least another three to four antibodies

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in addition to those presented previously (p. 190). In a separate study,
antibodies to beta-casein, another cow's milk protein, were significantly
elevated in bottle-fed infants compared to breast-fed infants; children
with Type 1 diabetes also had higher levels of these antibodies. 37 In
short, of the studies that have reported results, the findings strongly
confirm the danger of cow's milk, especially for genetically susceptible
children.

THE CONTROVERSY OF CONTROVERSY

Imagine looking at the front page of the newspaper and finding the
following headline: "Cow's Milk the Likely Cause of Lethal Type 1
Diabetes." Because the reaction would be so strong, and the economic
impact monumental, this headline won't be written anytime soon,
regardless of the scientific evidence. Stifling this headline is accom-
plished under the powerful label of "controversy." With so much at
stake, and so much information understood by so few people, it is easy
to generate and sustain controversy. Controversies are a natural part
of science. Too often, however, controversy is not the result of legiti-
mate scientific debate, but instead reflects the perceived need to delay
and distort research results. For example, if I say cigarettes are bad for
you and provide a mountain of evidence to support my contention,
the tobacco companies might come along and pick out one unsolved
detail and then claim that the whole idea of cigarettes being unhealthy
is mired in controversy, thereby nullifying all my conclusions. This is
easy to do, because there will always be unsolved details; this is the
nature of science. Some groups use controversy to stifle certain ideas,
impede constructive research, confuse the public and turn public
policy into babble rather than substance. Sustaining controversy as a
means of discrediting findings that cause economic or social discom-
fort is one of the greatest sins in science.

It can be difficult for the layperson to assess the legitimacy of a highly
technical controversy such as that regarding cow's milk and Type 1 dia-
betes. This is true even if the layperson is interested in reading scientific
articles.

Take a recent scientific review 38 of the cow's milk-Type 1 diabetes
association. In ten human studies (all case-control) summarized in a
paper published as part of a "controversial topics series," 38 the authors
concluded that five of the ten studies showed a statistically significant
positive association between cow's milk and Type 1 diabetes and five did

AUTOIMMUNE DISEASES

193

not. Obviously, this at first seems to demonstrate considerable uncer-
tainty, going a long way to discredit the hypothesis,

However, the five studies that were counted as "negative" did not
show that cow's milk decreased Type 1 diabetes. These five studies
showed no statistically significant effect either way. In contrast, there
are a total of five statistically significant studies and all five showed the
same result: early cow's milk consumption is associated with increased
risk of Type 1 diabetes. There is only one chance in sixty-four that this
was a random or chance result.

There are many, many reasons, some seen and some unseen, why an
experiment would find no statistically significant relationship between
two factors, even when a relationship really exists. Perhaps the study
didn't include enough people, and statistical certainty was unattainable.
Perhaps most of the subjects had very similar feeding practices, limiting
detection of the relationship you might otherwise see. Maybe trying to
measure infant feeding practices from years ago was inaccurate enough
that it obscured the relationship that does exist. Perhaps the researchers
were studying the wrong period of time in an infant's life.

The point is, if five of the ten studies did find a statistically significant
relationship, and all five showed that cow's milk consumption is linked
to increasing Type 1 diabetes, and none show that cow's milk consump-
tion is linked to decreasing Type 1 diabetes, I could hardly justify say-
ing, as the authors of this review did, that the hypothesis "has become
quite murky with inconsistencies in the literature." 38

In this same review, 38 the authors summarized additional studies that
indirectly compared breast-feeding practices associated with cow's milk
consumption and Type 1 diabetes. This compilation involved fifty-two
possible comparisons, twenty of which were statistically significant. Of
these twenty significant findings, nineteen favored an association of cow's
milk with disease, and only one did not. Again the odds heavily favored the
hypothesized association, something that the authors failed to note.

I cite this example not only to support the evidence showing a cow's
milk effect on Type 1 diabetes, but also to illustrate one tactic that is
often used to make something controversial when it is not. This practice
is more common than it should be and is a source of unnecessary con-
fusion. When researchers do this — even if they do it unintentionally —
they often have a serious prejudice against the hypothesis in the first
place. Indeed, shortly after I wrote this, I heard a brief National Public
Radio interview on the Type 1 diabetes problem with the senior author

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THE CHINA STUDY

of this review paper. 38 Suffice it to say, the author did not acknowledge
the evidence for the cow's milk hypothesis.

Because this issue has mammoth financial implications for American
agriculture, and because so many people have such intense personal
biases against it, it is unlikely that this diabetes research will reach the
American media anytime soon. However, the depth and breadth of evi-
dence now implicating cow's milk as a cause of Type 1 diabetes is over-
whelming, even though the very complex mechanistic details are not
yet fully understood. We not only have evidence of the danger of cow's
milk, we also have considerable evidence showing that the association
between diabetes and cow's milk is biologically plausible. Human breast
milk is the perfect food for an infant, and one of the most damaging
things a mother can do is to substitute the milk of a cow for her own.

MULTIPLE SCLEROSIS
AND OTHER AUTOIMMUNE DISEASES

Multiple sclerosis (MS) is a particularly difficult autoimmune disease,
both for those who have it and for those who care for its victims. It is a
lifelong battle involving a variety of unpredictable and serious disabilities.
MS patients often pass through episodes of acute attacks while gradually
losing their ability to walk or to see. After ten to fifteen years, they often
are confined to a wheelchair, and then to a bed for the rest of their lives.

About 400,000 people in the U.S. alone have the disease, according
to the National Multiple Sclerosis Society. 39 It is a disease that is initially
diagnosed between twenty and forty years of age and strikes women
about three times more often than men.

Even though there is widespread medical and scientific interest in
this disease, most authorities claim to know very little about causes
or cures. Major multiple sclerosis Internet Web sites all claim that the
disease is an enigma. They generally list genetics, viruses and environ-
mental factors as possibly playing roles in the development of this dis-
ease but pay almost no heed to a possible role for diet. This is peculiar
considering the wealth of intriguing information on the effects of food
that is available from reputable research reports. 40 ^ 2 Once again cow's
milk appears to play an important role.

The "multiple" symptoms of this disease represent a nervous system
gone awry. The electrical signals carrying messages to and from the
central nervous system (brain and spinal cord) and out through the pe-
ripheral nervous system to the rest of the body are not well coordinated

AUTOIMMUNE DISEASES

195

and controlled. This is because the insulating cover or sheath of the
nerve fibers, the myelin, is being destroyed by an autoimmune reaction.
Think of what would happen to your household wiring if the electrical
insulation became thin or was stripped away, leaving bare wires. The
electrical signals would be short-circuited. That is what happens with
MS; the wayward electrical signals may destroy cells and "burn" patches
of neighboring tissue, leaving little scars or bits of sclerotic tissue. These
"burns" can become serious and ultimately destroy the body.

The initial research showing an effect of diet on MS goes back more
than half a century to the research of Dr. Roy Swank, who began his
work in Norway and at the Montreal Neurological Institute during the
1940s. Later, Dr. Swank headed the Division of Neurology at the Uni-
versity of Oregon Medical School. 43

Dr. Swank became interested in the dietary connection when he
learned that MS appeared to be more common in the northern cli-
mates. 43 There is a huge difference in MS prevalence as one moves away
from the equator: MS is over 100 times more prevalent in the far north
than at the equator, 10 and seven times more prevalent in south Australia
(closer to the South Pole) than in north Australia. 44 This distribution is
very similar to the distribution of other autoimmune diseases, including
Type 1 diabetes and rheumatoid arthritis. 45, 46

Although some scientists speculated that magnetic fields might be
responsible for the disease, Dr. Swank thought it was diet, especially
animal-based foods high in saturated fats. 43 He found that inland dairy-
consuming areas of Norway had higher rates of MS than coastal fish-con-
suming areas.

Dr. Swank conducted his best-known trial on 144 MS patients re-
cruited from the Montreal Neurological Institute. He kept records on
these patients for the next thirty-four years. 47 He advised his patients
to consume a diet low in saturated fat, most of whom did, but many
of whom did not. He then classified them as good dieters or poor diet-
ers, based on whether they consumed less than 20 g/day or more than
20 g/day of saturated fat. (For comparison, a bacon cheeseburger with
condiments has about sixteen grams of saturated fat. One small frozen
chicken pot pie has almost ten grams of saturated fat.)

As the study continued, Dr. Swank found that progression of disease
was greatly reduced by the low-saturated fat diet, which worked even
for people with initially advanced conditions. He summarized his work
in 1990, 47 concluding that for the sub-group of patients who began the

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THE CHINA STUDY

CHART 9.4: MS DEATH RATE AFTER 144 PATIENTS DIETED
FOR THIRTY-FOUR YEARS

70%

60%-

50% -

Percent who
died of MS

40%-

30%-

20%-

10%-

Poor Dieters

Good Dieters

low-saturated fat diet during the earlier stages of their disease, "about
95%. . .remained only mildly disabled for approximately thirty years."
Only 5% of these patients died. In contrast, 80% of the patients with early-
stage MS who consumed the "poor" diet (higher saturated fat) died of MS.
The results from all 144 patients, including those who started the diet
at a later stage of disease, are shown in Chart 9.4.

This work is remarkable. To follow people for thirty-four years is an
exceptional demonstration of perseverance and dedication. Moreover,
if this were a study testing a potential drug, these findings would make
any pharmaceutical manufacturer jingle the coins in his or her pocket.
Swank's first results were published more than a half century ago, 48 then
again 49 and again 50 and again 47 for the next forty years.

More recently, additional studies 42 51,52 have confirmed and extended
Swank's observations and gradually have begun to place more empha-
sis on cow's milk. These new studies show that consuming cow's milk
is strongly linked to MS both when comparing different countries 52
and when comparing states within the U.S. 51 Chart 9.5, published by
French researchers, compares the consumption of cow's milk with MS
for twenty-six populations in twenty-four countries. 52

This relationship, which is virtually identical to that for Type 1
diabetes, is remarkable, and it is not due to variables such as the avail-
ability of medical services or geographic latitude. 51 In some studies 52 ' 53
researchers suggest this strong correlation with fresh cow's milk might

AUTOIMMUNE DISEASES 197

CHART 9.5: ASSOCIATION OF COW'S MILK CONSUMPTION
AND MULTIPLE SCLEROSIS

200 -i

0 100

Milk Consumption (kg/inhabitants/year)

be due to the presence of a virus in the milk. These more recent studies
also suggest that saturated fat alone probably was not fully responsible
for Swank's results. The consumption of meat high in saturated fat, like
milk, was also associated with MS in these multi-country studies, 5 ''
while the consumption of fish, containing more omega-3 fat, was as-
sociated with low rates of disease. 55

The association of cow's milk with MS, shown in Chart 9.5, may be
impressive, but it does not constitute proof. For example, where do
genes and viruses come into play? Each of these, in theory, might ac-
count for the unusual geographic distribution of this disease.

In the case of viruses, no definite conclusions are yet possible. A
variety of different virus types have been suggested and a variety of ef-
fects on the immune system may be involved. However, nothing very
convincing has been proven. Some of the evidence is based on finding
more viral antibodies in MS patients than in controls, some is based on
sporadic outbreaks of MS among isolated communities, and some is
based on finding virus-like genes among MS cases. 13, 19,56

With regard to genes, we can begin to puzzle out their association
with MS by asking the usual question: what happens to people who
migrate from one population to another, keeping their genes the same

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THE CHINA STUDY

but changing their diets and their environment? The answer is the same
as it was for cancer, heart disease and Type 2 diabetes. People acquire
the risk of the population to which they move, especially if they move
before their adolescent years. 57, 58 This tells us that this disease is more
strongly related to environmental factors than it is to genes. 59

Specific genes have been identified as possible candidates for causing
MS but, according to a recent report, 3 there may be as many as twenty-
five genes playing such a role. Therefore, it will undoubtedly be a long
time before we determine with any precision which genes or combina-
tions of genes predispose someone to MS. Genetic predisposition may
make a difference as to who gets MS, but even at best, genes can only
account for about one-fourth of the total disease risk. 60

Although MS and Type 1 diabetes share some of the same unanswered
questions on the exact roles of viruses and genes and the immune sys-
tem, they also share the same alarming evidence regarding diet. For
both diseases, a "Western" diet is strongly associated with disease in-
cidence. Despite the efforts of those who would rather dismiss or mire
these observational studies in controversy, they paint a consistent pic-
ture. Intervention studies conducted on people already suffering from
these diseases only reinforce the findings of the observational studies.
Dr. Swank did brilliant work on MS, and you may recall from chapter
seven that Dr. James Anderson successfully reduced the medication re-
quirements for Type 1 diabetics using diet alone. It's important to note
that both of these doctors used a diet that was significantly more mod-
erate than a total whole foods, plant-based diet. I wonder what would
happen to these autoimmune patients if the ideal diet were followed. I
would bet on even greater success.

THE COMMONALITY OF AUTOIMMUNE DISEASES

What about other autoimmune diseases? There are dozens of autoim-
mune diseases and I have mentioned only two of the more prominent
ones. Can we say anything about autoimmune diseases as a whole?

To answer this question, we need to identify how much these dis-
eases have in common. The more they have in common, the greater the
probability that they also will share a common cause (or causes). This
is like seeing two people you don't know, both of whom have a similar
body type, hair color, eye color, facial features, physical and vocal man-
nerisms and age, and concluding that they come from the same parents.
Just as we hypothesized that diseases of affluence such as cancer and

AUTOIMMUNE DISEASES

199

heart disease have common causes because they share similar geogra-
phy and similar biochemical biomarkers (chapter four), we can also
hypothesize that MS, Type 1 diabetes, rheumatoid arthritis, lupus and
other autoimmune diseases may share a similar cause if they exhibit
similar characteristics.

First, by definition, each of these diseases involves an immune sys-
tem that has gone awry in such a way that it attacks "self' proteins that
look the same as foreign proteins.

Second, all the autoimmune diseases that have been studied have
been found to be more common at the higher geographic latitudes
where there is less constant sunshine. 910 - 61

Third, some of these diseases have a tendency to afflict the same
people. MS and Type 1 diabetes, for example, have been shown to coex-
ist in the same individuals. 62-65 Parkinson's disease, a non-autoimmune
disease with autoimmune characteristics, is often found with MS, both
within the same geographic regions 66 and within the same individuals. 5
MS also has been associated — either geographically or within the same
individuals — with other autoimmune diseases like lupus, myasthenia
gravis, Graves' disease and eosinophilic vasculitis. 63 Juvenile rheuma-
toid arthritis, another autoimmune disease, has been shown to have an
unusually strong association with Hashimoto thyroiditis. 67

Fourth, of those diseases studied in relation to nutrition, the con-
sumption of animal-based foods — especially cow's milk — is associated
with greater disease risk.

Fifth, there is evidence that a virus (or viruses) may trigger the onset
of several of these diseases.

A sixth and most important characteristic binding together these
diseases is the evidence that their "mechanisms of action" have much
in common — jargon used to describe the "how to" of disease forma-
tion. As we consider common mechanisms of action, we might start
with sunlight exposure, because this somehow seems linked to the au-
toimmune diseases. Sunlight exposure, which decreases with increas-
ing latitude, could be important — but clearly there are other factors.
The consumption of animal-based foods, especially cow's milk, also
increases with distance from the equator. In fact, in one of the more ex-
tensive studies, cow's milk was found to be as good of a predictor of MS
as latitude (i.e., sunshine). 51 In Dr. Swank's studies in Norway, MS was
less common near the coastal areas of the country where fish intake was
more common. This gave rise to the idea that the omega-3 fats common

200

THE CHINA STUDY

to fish might have a protective effect. What is almost never mentioned,
however, is that dairy consumption (and saturated fat) was much lower
in the fish-eating areas. Is it possible that cow's milk and lack of sun-
shine are having a similar effect on MS and other autoimmune diseases
because they operate through a similar mechanism? This could be very
interesting, if true.

As it turns out, the idea is not so crazy. This mechanism involves,
once again, vitamin D. There are experimental animal models of lupus,
MS, rheumatoid arthritis and inflammatory bowel disease (e.g., Crohn's
disease, ulcerative colitis), each of which is an autoimmune disease. 6 - 768
Vitamin D, operating through a similar mechanism in each case, prevents
the experimental development of each of these diseases. This becomes
an even more intriguing story when we think about the effect of food on
vitamin D.

The first step in the vitamin D process occurs when you go outside
on a sunny day. When the sunshine hits your exposed skin, the skin
produces vitamin D. The vitamin D then must be activated in the kid-
ney in order to produce a form that helps repress the development of
autoimmune diseases. As we've seen before, this critically important
activation step can be inhibited by foods that are high in calcium and
by acid-producing animal proteins like cow's milk (some grains also
produce excess acid). Under experimental conditions, the activated
vitamin D operates in two ways: it inhibits the development of certain
T-cells and their production of active agents (called cytokines) that
initiate the autoimmune response, and/or it encourages the production
of other T-cells that oppose this effect. 69 ' 70 (An abbreviated schematic
of this vitamin D network is shown in Appendix C.) This mechanism
of action appears to be a strong commonality between all autoimmune
diseases so far studied.

Knowing the strength of the evidence against animal foods, cow's milk
in particular, for both MS and Type 1 diabetes, and knowing how much
in common all of the autoimmune diseases have, it is reasonable to be-
gin thinking about food and its relationship to a much broader group of
autoimmune diseases. Obviously caution is called for; more research is
needed to make conclusive statements about cross-autoimmune disease
similarities. But the evidence we have now is already striking.

Today almost no indication of the dietary connection to these dis-
eases has reached public awareness. The Web site of the Multiple Scle-
rosis International Federation, for example, reads, "There is no credible

AUTOIMMUNE DISEASES

201

evidence that MS is due to poor diet or dietary deficiencies." They warn
that dietary regimens can be "expensive" and "can alter the normal
nutritional balance." 71 If changing your diet is expensive, I don't know
what they would say about being bedridden and incapacitated. As far as
altering the "normal nutritional balance" is concerned, what is normal?
Does this mean the diet that we now eat is "normal" — the diet that is
largely responsible for diseases that cripple, kill and make profoundly
miserable millions of Americans every year? Are massive rates of heart
disease, cancer, autoimmune diseases, obesity and diabetes "normal"? If
this is normal, I propose we start seriously considering the abnormal.

There are 400,000 Americans who are victims of multiple sclerosis,
and millions more with other autoimmune diseases. While statistics,
research results and clinical descriptions form the basis for much of my
discussion of diet and disease, the importance of the information comes
down to the intimate experience of individual people. Any one of these
serious diseases I've talked about in this chapter can forever alter the
life of any person — a family member, a friend, a neighbor, a coworker
or you yourself.

It is time to sacrifice our sacred cows. Reason must prevail. Profes-
sional societies, doctors and government agencies need to stand up and
do their duty, so that children being born today do not face tragedies
that otherwise could be prevented.

_ 10

Wide-Ranging Effects:
Bone, Kidney, Eye
and Brain Diseases

One of the most convincing arguments for a plant-based diet is the fact
that it prevents a broad range of diseases. If I have a conversation with
someone about a single study showing the protective effect of fruits
and vegetables on heart disease, they may agree that it's all very nice for
fruits and vegetables, but they will probably still go home to meatloaf
and gravy. It doesn't matter how big the study, how persuasive the re-
sults or how respectable the scientists who conducted the investigation.
The fact is that most people have a healthy skepticism about one study
standing alone — as well they should.

But if I tell them about dozens and dozens of studies showing that the
countries with low rates of heart disease consume low amounts of animal-
based foods, and dozens and dozens of studies showing that individuals
who eat more whole, plant-based foods get less heart disease, and I go on
to document still more studies showing that a diet low in animal-based
foods and high in unprocessed plant-based foods can slow or reverse
heart disease, then people are more inclined to pay some attention.

If I keep talking and go through this process not only for heart dis-
ease, but obesity, Type 2 diabetes, breast cancer, colon cancer, prostate

203

204

THE CHINA STUDY

cancer, multiple sclerosis and other autoimmune diseases, it's quite pos-
sible that people may never eat meatloaf and gravy again.

What has become so convincing about the effect of diet on health is
the breadth of the evidence. While a single study might be found to sup-
port almost any idea under the sun, what are the chances that hundreds,
even thousands, of different studies show a protective benefit of plant-
based foods and/or harmful effects of animal-based foods for so many
different diseases? We can't say it's due to coincidence, bad data, biased
research, misinterpreted statistics or "playing with numbers." This has
got to be the real deal.

I have so far presented only a small sample of the breadth of evidence
that supports plant-based diets. To show you just how broad this evi-
dence is, I will cover five more seemingly unrelated diseases common
in America: osteoporosis, kidney stones, blindness, cognitive dysfunc-
tion and Alzheimer's disease. These disorders are not often fatal and are
often regarded as the inevitable consequences of aging. Therefore, we
don't think it's unnatural when grandpa gets blurry spots in his vision,
can't remember the names of his friends or needs a hip replacement op-
eration. But, as we shall see, even these diseases have a dietary link.

OSTEOPOROSIS

Did you ever have an elementary school teacher tell you that if you
didn't have bones, you would just be a shapeless blob on the floor? Or
maybe you learned about the human skeleton from that popular song,
"... the ankle bone is connected to the shin bone, the shin bone is con-
nected to the knee bone," etc. At that same time in your life, you prob-
ably were told to drink milk to build strong bones and teeth. Because
none of us want to be shapeless blobs, and because our celebrities have
been paid to advertise milk's presumed benefits, we drank it. Milk is to
bone health as bees are to honey.

Americans consume more cow's milk and its products per person
than most populations in the world. So Americans should have wonder-
fully strong bones, right? Unfortunately not. A recent study showed that
American women aged fifty and older have one of the highest rates of hip
fractures in the world. 1 The only countries with higher rates are in Europe
and in the south Pacific (Australia and New Zealand) 1 where they con-
sume even more milk than the United States. What's going on?

An excess rate of hip fractures is often used as a reliable indicator of
osteoporosis, a bone disease that especially affects women after meno-

WIDE-RANGING EFFECTS: BONE, KIDNEY, EYE, BRAIN DISEASES 205

pause. It is often claimed to be due to an inadequate intake of calcium.
Therefore, health policy people often recommend higher calcium con-
sumption. Dairy products are particularly rich in calcium, so the dairy
industry eagerly supports efforts to boost calcium consumption. These
efforts have something to do with why you were told to drink your milk
for strong bones — the politics of which are discussed in Part IV

Something is amiss, though, because those countries that use the
most cow's milk and its products also have the highest fracture rates and
the worst bone health. One possible explanation is found in a report
showing an impressively strong association between animal protein
intake and bone fracture rate for women in different countries. 2 Au-
thored in 1992 by researchers at Yale University School of Medicine, the
report summarized data on protein intake and fracture rates taken from
thirty-four separate surveys in sixteen countries that were published
in twenty-nine peer-reviewed research publications. All the subjects in
these surveys were women fifty years and older. It found that a very
impressive 70% of the fracture rate was attributable to the consumption
of animal protein.

These researchers explained that animal protein, unlike plant pro-
tein, increases the acid load in the body 3 An increased acid load means
that our blood and tissues become more acidic. The body does not like
this acidic environment and begins to fight it. In order to neutralize the
acid, the body uses calcium, which acts as a very effective base. This
calcium, however, must come from somewhere. It ends up being pulled
from the bones, and the calcium loss weakens them, putting them at
greater risk for fracture.

We have had evidence for well over a hundred years that animal pro-
tein decreases bone health. The explanation of animal protein causing
excess metabolic acid, for example, was first suggested in the 1880s''
and was documented as long ago as 1920. 5 We also have known that
animal protein is more effective than plant protein at increasing the
metabolic acid load in the body 6 7 8

When animal protein increases metabolic acid and draws calcium
from the bones, the amount of calcium in the urine is increased. This
effect has been established for over eighty years 5 and has been studied
in some detail since the 1970s. Summaries of these studies were pub-
lished in 1974, 9 1981 10 and 1990. 11 Each of these summaries clearly
shows that the amount of animal protein consumed by many of us on
a daily basis is capable of causing substantial increases in urinary cal-

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THE CHINA STUDY

CHART 10.1: ASSOCIATION OF URINARY CALCIUM EXCRETION
WITH DIETARY PROTEIN INTAKE

% Increase in Protein Intake

cium. Chart 10.1 is taken from the 1981 publication. 10 Doubling protein
intake (mostly animal-based) from 35-78 g/day causes an alarming 50%
increase in urinary calcium. This effect occurs well within the range
of protein intake that most of us consume; average American intake is
around 70-100 g/day Incidentally as mentioned in chapter four, a six-
month study funded by the Atkins Center found that those people who
adopted the Atkins Diet excreted 50% more calcium in their urine after
six months on the diet. 12

The initial observations on the association between animal protein
consumption and bone fracture rates are very impressive, and now we
have a plausible explanation as to how the association might work, a
mechanism of action.

Disease processes are rarely as simple as "one mechanism does it all,"
but the work being done in this field makes a strong argument. A more
recent study published in 2000, comes from the Department of Medi-
cine at the University of California at San Francisco. Using eighty-seven
surveys in thirty-three countries, it compared the ratio of vegetable to
animal protein consumption to the rate of bone fractures (Chart 10. 2). 1
A high ratio of vegetable to animal protein consumption was found to
be impressively associated with a virtual disappearance of bone frac-
tures.

These studies are compelling for several reasons. They were published
in leading research journals, the authors were careful in their analyses and

WIDE-RANGING EFFECTS: BONE, KIDNEY, EYE, BRAIN DISEASES 207

CHART 10.2: ASSOCIATION OF ANIMAL VERSUS PLANT PROTEIN
INTAKE AND BONE FRACTURE RATES FOR DIFFERENT COUNTRIES

I — i i I l l ■ '

0.0 1.0 2.0 3.0 4.0 5.0 6.0

Vegetable-to-Animal Protein Intake Ratio (g/g)

interpretation of data, they included a large number of individual research
reports, and the statistical significance of the association of animal protein
with bone fracture rates is truly exceptional. They cannot be dismissed as
just another couple of studies; the most recent study represents a sum-
mary of eighty-seven separate surveys!

The Study of Osteoporotic Fractures Research Group at the Univer-
sity of California at San Francisco published yet another study 13 of over
1,000 women aged sixty-five and up. Like the multi-country study, re-
searchers characterized women's diets by the proportions of animal and
plant protein. After seven years of observations, the women with the
highest ratio of animal protein to plant protein had 3.7 times more bone
fractures than the women with the lowest ratio. Also during this time
the women with the high ratio lost bone almost four times as fast as the
women with the lowest ratio.

Experimentally, this study is high quality because it compared pro-
tein consumption, bone loss and broken bones for the same subjects.
This 3.7-fold effect is substantial, and is very important because the

208

THE CHINA STUDY

women with the lowest bone fracture rates still consumed, on average,
about half of their total protein from animal sources. I can't help but
wonder how much greater the difference might have been had they con-
sumed not 50% but 0-10% of their total protein from animal sources. In
our rural China study, where the animal to plant ratio was about 10%,
the fracture rate is only one-fifth that of the U.S. Nigeria shows an ani-
mal-to-plant protein ratio only about 10% that of Germany and the hip
fracture incidence is lower by over 99%.'

These observations raise a serious question about the widely adver-
tised claim that protein-rich dairy foods protect our bones. And yet we
still are warned almost daily about our need for dairy foods to provide
calcium for strong bones. An avalanche of commentary warns that most
of us are not meeting our calcium requirements, especially pregnant and
lactating women. This calcium bonanza, however, is not justified. In
one study of ten countries, 14 a higher consumption of calcium was as-
sociated with a higher — not lower — risk of bone fracture (Chart 10.3).
Much of the calcium intake shown in this chart, especially in high con-
sumption countries, is due to dairy foods, rather than calcium supple-
ments or non-dairy food sources of calcium.

Mark Hegsted, who produced the results in Chart 10.3, was a long-
time Harvard professor. He worked on the calcium issue beginning in the
early 1950s, was a principal architect of the nation's first dietary guide-
lines in 1980 and in 1986 published this graph. Professor Hegsted be-
lieves that excessively high intakes of calcium consumed over a long time
impair the body's ability to control how much calcium it uses and when.
Under healthy conditions, the body uses an activated form of vitamin
D, calcitriol, to adjust how much calcium it absorbs from food and how
much it excretes and distributes in the bone. Calcitriol is considered a
hormone; when more calcium is needed, it enhances calcium absorption
and restricts calcium excretion. If too much calcium is consumed over a
long period of time, the body may lose its ability to regulate calcitriol, per-
manently or temporarily disrupting the regulation of calcium absorption
and excretion. Ruining the regulatory mechanism in this way is a recipe
for osteoporosis in menopausal and post-menopausal women. Women at
this stage of life must be able to enhance their utilization of calcium in a
timely manner, especially if they continue to consume a diet high in ani-
mal protein. The fact that the body loses its ability to control finely tuned
mechanisms when they are subjected to continuous abuse is a well-estab-
lished phenomenon in biology.

WIDE-RANGING EFFECTS: BONE, KIDNEY, EYE, BRAIN DISEASES 209

CHART 10.3: ASSOCIATION OF RATES OF HIP FRACTURES
WITH CALCIUM INTAKE FOR DIFFERENT COUNTRIES

120

100

o
o
o
o
o

- 80

! 60 -

c
-a

40 -

20 -

• UNITED STATES

• NEW ZEALAND

• SWEDEN

• JERUSALEM

• UNITED KINGDOM

• HOLLAND

• YUGOSLAVIA
• HONG KONG

• SINGAPORE

• FINLAND

I I

500 1,000
Calcium Consumption (mg/day)

1,500

Given these findings, it seems perfectly plausible that animal protein
and even calcium — when consumed at excessive levels — are capable of
increasing the risk of osteoporosis. Dairy, unfortunately is the only food
that is rich in both of these nutrients. Hegsted, backed by his excep-
tional experience in calcium research, said in his 1986 paper, "...hip
fractures are more frequent in populations where dairy products are
commonly consumed and calcium intakes are relatively high."

Years later, the dairy industry still suggests that we should be consum-
ing more of its products to build strong bones and teeth. The confusion,
conflict and controversy rampant in this area of research allow anybody
to say just about anything. And of course, huge amounts of money are at
stake as well. One of the most cited osteoporosis experts — one funded
by the dairy industry — angrily wrote in a prominent editorial 15 that the
findings favoring a diet with a higher ratio of plant-to-animal protein
cited above could have been "influenced to some extent by currents in

210

THE CHINA STUDY

the larger society." The "currents" he was referring to were the animal
rights activists opposed to the use of dairy foods.

Much of the debate regarding osteoporosis, whether it is conducted
with integrity or otherwise, resides in the research concerning the de-
tails. As you shall see, the devil lurks in the details, the primary detail
being that of bone mineral density (BMD).

Many scientists have investigated how various diet and lifestyle fac-
tors affect BMD. BMD is a measure of bone density that is often used to
diagnose bone health. If your bone density falls below a certain level,
you may be at risk for osteoporosis. In practical terms, this means that
if you have a low BMD, you are at a higher risk for a fracture. 1 ^ 18 But
there are some devilishly contradictory and confusing details in this
great circus of osteoporosis research. To name a few:

• A high BMD increases the risk of osteoarthritis. 19

• A high BMD has been linked to a higher risk of breast cancer. 20 21

• Although high BMD is linked both to increased breast cancer risk
and decreased osteoporotic risk, breast cancer and osteoporosis
nonetheless cluster together in the same areas of the world and
even in the same individuals. 22

• Rate of bone loss matters just as much as overall BMD. 23

• There are places where overall bone mass, bone mineral density
or bone mineral content measurements are lower than they are in
"Western" countries, but the fracture rate also is lower, defying ac-
cepted logic of how we define "big, strong bones. " 24_2e

• Being fat is linked to greater BMD, 24, 27 even though areas of the
world that have higher rates of obesity also have higher rates of
osteoporosis.

Something is wrong with the idea that BMD reliably represents os-
teoporosis and, by inference, indicates the kind of diet that would lower
fracture rates. In contrast, an alternative, but much better, predictor
of osteoporosis is the dietary ratio of animal-to-plant protein. 1 ' 13 The
higher the ratio, the higher the risk of disease. And guess what? BMD is
not significantly associated with this ratio. 13

Clearly the conventional recommendations regarding animal foods,
dairy and bone mineral density, which are influenced and advertised by
the dairy industry, are besieged by serious doubts in the literature. Here
is what I would recommend you do, based on the research, to minimize
your risk of osteoporosis:

WIDE-RANGING EFFECTS: BONE, KIDNEY, EYE, BRAIN DISEASES 211

• Stay physically active. Take the stairs instead of the elevator, go for
walks, jogs, bicycle rides. Swim, do yoga or aerobics every couple
of days and don't be afraid to buy barbells to use once in a while.
Play a sport or join a social group that incorporates exercise. The
possibilities are endless, and they can be fun. You'll feel better, and
your bones will be much healthier for the effort.

• Eat a variety of whole plant foods, and avoid animal foods, includ-
ing dairy. Plenty of calcium is available in a wide range of plant
foods, including beans and leafy vegetables. As long as you stay
away from refined carbohydrates, like sugary cereals, candies,
plain pastas and white breads, you should have no problem with
calcium deficiency.

• Keep your salt intake to a minimum. Avoid highly processed and
packaged foods, which contain excess salt. There is some evidence
that excessive salt intake can be a problem.

KIDNEYS

At the Web site for the UCLA Kidney Stone Treatment Center, 28 you will
discover that kidney stones may cause the following symptoms:

• Nausea, vomiting

• Restlessness (trying to find comfortable position to ease the pain)

• Dull pain (ill-defined, lumbar, abdominal, intermittent pain)

• Urgency (urge to empty the bladder)

• Frequency (frequent urination)

• Bloody urine with pain (gross hematuria)

• Fever (when complicated by infection)

• Acute renal colic (severe colicky flank pain radiating to groin, scro-
tum, labia)

Acute renal colic deserves some explanation. This agonizing symp-
tom is the result of a crystallized stone trying to pass through the thin
tube in your body (ureter) that transports urine from the kidney to the
bladder. In describing the pain involved, the Web site states, "This is
probably one of the worst pains humans experience. Those who have

had it will never forget it The severe pain of renal colic needs to be

controlled by potent pain killers. Don't expect an aspirin to do the trick.
Get yourself to a doctor or an emergency room." 28

I don't know about you, but just thinking about these things gives me

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a shiver. Unfortunately, up to 15% of Americans, more men than wom-
en, will be diagnosed with having a kidney stone in their lifetime. 29

There are several kinds of kidney stones. Although one is a geneti-
cally rare type 30 and another is related to urinary infection, the major-
ity involve stones made of calcium and oxalate. These calcium oxalate
stones are relatively common in developed countries and relatively rare
in developing countries. 31 Again, this illness falls into the same global
patterns as all the other Western diseases.

I first was made aware of the dietary connection with this disease at
the Faculty of Medicine of the University of Toronto. I was invited to
give a seminar on our China Study findings and while there I met Pro-
fessor W. G. Robertson from the Medical Research Council in Leeds,
England. This chance encounter was extremely rewarding. Dr. Robert-
son, as I have come to learn, is one of the world's foremost experts on
diet and kidney stones. Dr. Robertson's research group has investigated
the relationship between food and kidney stones with great depth and
breadth, both in theory and in practice. Their work began more than
thirty years ago and continues to the present day. A search of the scien-
tific publications authored or co-authored by Robertson shows at least
100 papers published since the mid-1960s.

One of Robertson's charts depicts a stunning relationship between
animal protein consumption and the formation of kidney stones (Chart
10.4). 32 It shows that consuming animal protein at levels above twenty-
one grams per person per day (slightly less than one ounce) for the
United Kingdom for the years of 1958 to 1973 is closely correlated with
a high number of kidney stones formed per 10,000 individuals per year.
This is an impressive relationship.

Few researchers have worked out the details of a research ques-
tion more thoroughly than Robertson and his colleagues. They have
developed a model for estimating the risk of stone formation with re-
markable accuracy. 33 Although they have identified six risk factors for
kidney stones, 34 ' 35 animal protein consumption was the major culprit.
Consumption of animal protein at levels commonly seen in affluent
countries leads to the development of four of the six risk factors. 34, 35

Not only is animal protein linked to risk factors for future formation
of stones, but it affects recurring stones as well. Robertson published
findings showing that, among the patients who had recurrent kidney
stones, he was able to resolve their problem simply by shifting their diet
away from animal protein foods. 36

WIDE-RANGING EFFECTS: BONE, KIDNEY, EYE, BRAIN DISEASES 213

CHART 10.4: ASSOCIATION BETWEEN ANIMAL PROTEIN INTAKE
AND FORMATION OF URINARY CALCULI

20 21 22 23 24 25

Meat, Fish and Poultry Protein Intake (g/head/day)

How does this work? When enough animal protein-containing foods
are consumed, the concentrations of calcium and oxalate in the urine
increase sharply, usually within hours. Chart 10.5 shows these impres-
sive changes, published by Robertson's group. 35

The individuals in this study consumed only fifty-five grams per day
of animal protein, to which was added another thirty-four grams per
day of animal protein in the form of tuna fish. This amount of animal
protein consumption is well within the levels most Americans regularly
eat. Men consume around 90-100 grams of total protein per day, the
majority of which comes from animal foods; women consume about
70-90 grams per day.

When the kidney is under a persistent, long-term assault from in-
creased calcium and oxalate, kidney stones may result. 35 The following,
excerpted from a 1987 review by Robertson, 37 emphasizes the role of
diet, especially foods containing animal proteins:

Urolithiasis [kidney stone formation] is a worldwide problem
which appears to be aggravated by the high dairy-produce, highly
energy-rich and low-fibre diets consumed in most industrialized

countries Evidence points, in particular, to a high-meat protein

intake as being the dominant factor On the basis of epidemio-
logical and biochemical studies a move toward a more vegetarian,
less energy-rich diet would be predicted to reduce the risk of stone
in the population.

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CHART 10.5: EFFECT OF ANIMAL PROTEIN INTAKE
ON CALCIUM AND OXALATE IN THE URINE

Calcium Oxalate

'A 6 8 10 12

+ Animal Protein

\A 6 8 10 12
+ Animal Protein

A substantial and convincing effect on stone formation has been dem-
onstrated for animal-based foods. Recent research also shows that kidney
stone formation can be initiated by the activity of free radicals, 38 and may
thus be prevented by consumption of antioxidant-containing plant-based
foods (see chapter four). For yet another organ and another disease, we
see opposing effects (in this case on stone formation) by animal- and
plant-based foods.

EYE PROBLEMS

People who can see well often take vision for granted. We treat our
eyes more as little bits of technology than as living parts of the body,
and are all too willing to believe that lasers are the best course of action
for maintaining healthy eyes. But during the past couple of decades,
research has shown that these bits of "technology" are actually greatly
affected by the foods we eat. Our breakfasts, lunches and dinners have
a particular effect on two common eye diseases, cataracts and macular
degeneration — diseases which afflict millions of older Americans.

Yes, that's right. I'm about to tell you that if you eat animal foods in-
stead of plant foods, you just might go blind.

Macular degeneration is the leading cause of irreversible blindness

WIDE-RANGING EFFECTS: BONE, KIDNEY, EYE, BRAIN DISEASES 215

among people over age sixty-five. Over 1.6 million Americans suffer
from this disease, many of whom become blind. 39 As the name implies,
this condition involves destruction of the macula, which is the bio-
chemical intersection in the eye — where the energy of the light coming
in is transformed into a nerve signal. The macula occupies center stage,
so to speak, and it must be functional for sight to occur.

Around the macula there are fatty acids that can react with incoming
light to produce a low level of highly reactive free radicals. 40 These free
radicals (see chapter four) can destroy, or degenerate, neighboring tis-
sue, including the macula. But fortunately for us, free radical damage
can be repressed thanks to the antioxidants in vegetables and fruits.

Two studies, each involving a team of experienced researchers at
prestigious institutions, provide compelling evidence that food can pro-
tect against macular degeneration. Both studies were published a decade
ago. One evaluated diet 41 and the other assessed nutrients in blood. 42
The findings of these two studies suggested that as much as 70-88%
of blindness caused by macular degeneration could be prevented if the
right foods are eaten.

The study on dietary intakes 41 compared 356 individuals fifty-five to
eighty years of age who were diagnosed with advanced macular degen-
eration (cases) with 520 individuals with other eye diseases (controls).
Five ophthalmology medical centers collaborated on the study.

Researchers found that a higher intake of total carotenoids was as-
sociated with a lower frequency of macular degeneration. Carotenoids
are a group of antioxidants found in the colored parts of fruits and veg-
etables. When carotenoid intakes were ranked, those individuals who
consumed the most had 43% less disease than those who consumed the
least. Not surprisingly, five out of six plant-based foods measured also
were associated with lower rates of macular degeneration (broccoli, car-
rots, spinach or collard greens, winter squash and sweet potato). Spin-
ach or collard greens conferred the most protection. There was 88% less
disease for people who ate these greens five or more times per week
when compared with people who consumed these greens less than once
per month. The only food group not showing a preventive effect was the
cabbage/cauliflower/brussels sprout group, which sports the least color
of the six food groups. 43

These researchers also looked at the potential protection from dis-
ease as a result of the consumption of five of the individual carotenoids
consumed in these foods. All but one of these five showed a highly

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significant protective effect, especially the carotenoids found in the
dark green leafy vegetables. In contrast, supplements of a few vitamins,
including retinol (preformed "vitamin" A), vitamin C and vitamin E
showed little or no beneficial effects. Yet again, we see that while sup-
plements may give great wealth to supplement manufacturers, they will
not give great health to you and me.

When all was said and done, this study found that macular degenera-
tion risk could be reduced by as much as 88%, simply by eating the right
foods.' 1

At this point you may be wondering, "Where can I get some of those
carotenoids?" Green leafy vegetables, carrots and citrus fruits are all
good sources. Herein lies a problem, however. Among the hundreds
(maybe thousands) of antioxidant carotenoids in these foods, only a
dozen or so have been studied in relation to their biological effects. The
abilities of these chemicals to scavenge and reduce free radical damage
are well established, but the activities of the individual carotenoids vary
enormously depending on dietary and lifestyle conditions. Such varia-
tions make it virtually impossible to predict their individual activities,
either good or bad. The logic of using them as supplements is much too
particular and superficial. It ignores the dynamic of nature. It's much
safer to consume these carotenoids in their natural context, in highly
colored fruits and vegetables.

The second study 42 compared a total of 421 macular degeneration
patients (cases) with 615 controls. Five of the leading clinical centers
specializing in eye diseases and their researchers participated in this
study. The researchers measured the levels of antioxidants in the blood,
rather than the antioxidants consumed. Four kinds of antioxidants were
measured: carotenoids, vitamin C, selenium and vitamin E. Except for
selenium, each of these nutrient groups was associated with fewer cases
of macular degeneration, although only the carotenoids showed statisti-
cally significant results. Risk of macular degeneration was reduced by
two-thirds for those people with the highest levels of carotenoids in
their blood, when compared with the low-carotenoid group.

This reduction of about 65-70% in this study is similar to the reduc-
tion of upwards of 88% in the first study. These two studies consistently
demonstrated the benefits of antioxidant carotenoids consumed as
food. Given experimental limitations, we can only approximate the pro-
portion of macular degeneration caused by poor dietary habits, and we
cannot know which antioxidants are involved. What we can say, howev-

WIDE-RANGING EFFECTS: BONE, KIDNEY, EYE, BRAIN DISEASES 217

er, is that eating antioxidant-containing foods, especially those contain-
ing the carotenoids, will prevent most blindness cases resulting from
macular degeneration. This in itself is a remarkable recommendation.

Cataracts are slightly less serious than macular degeneration because
there are effective surgical options available to restore vision loss caused
by this disease. But when you look at the numbers, cataracts are a much
larger burden on our society. By the age of eighty, half of all Americans
will have cataracts. 39 Currently there are 20 million Americans age forty
and older with the disease.

Cataract formation involves the clouding of the eye lens. Corrective
surgery involves removing the cloudy lens and replacing it with an arti-
ficial lens. The development of the opaque condition, like the degenera-
tion of the macula and so many other disease conditions in our body, is
closely associated with the damage created by an excess of reactive free
radicals. 44 Once again, it is reasonable to assume that eating antioxi-
dant-containing foods should be helpful.

Starting in 1988, researchers in Wisconsin began to study eye health
and dietary intakes in over 1,300 people. Ten years later, they published
a report 45 on their findings. The people who consumed the most lutein,
a specific type of antioxidant, had one-half the rate of cataracts as the
people who consumed the least lutein. Lutein is an interesting chemical
because, in addition to being readily available in spinach, along with
other dark leafy green vegetables, it also is an integral part of the lens
tissue itself. 46, 47 Similarly, those who consumed the most spinach had
40% less cataracts.

These two eye conditions, macular degeneration and cataracts, both
occur when we fail to consume enough of the highly colored green and
leafy vegetables. In both cases, excess free radicals, increased by animal-
based foods and decreased by plant-based foods, are likely to be respon-
sible for these conditions.

MIND-ALTERING DIETS

By the time this book hits the shelves, I will be seventy years old. I
recently went to my high school's fiftieth reunion, where I learned that
many of my classmates had died. I receive the AARP magazine, get
discounts on various products for being advanced in age and receive
social security checks every month. Some euphemists might call me a
"mature adult." I just say old. What does it mean to be old? I still run
every morning, sometimes six or more miles a day. I still have an active

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work life, perhaps more active than ever. I still enjoy all the same leisure
activities, whether visiting grandchildren, dining with friends, garden-
ing, traveling, golfing, lecturing or making outdoor improvements like
building fences or tinkering with this or that as 1 used to do on the farm.
Some things have changed, though. Clearly there is a difference between
the seventy-year-old me and the twenty-year-old me. 1 am slower, not as
strong, work fewer hours every day and am prone to taking naps more
frequently than I used to.

We all know that getting old brings with it diminished capacities
compared with our younger days. But there is good science to show that
thinking clearly well into our later years is not something we need to
give up. Memory loss, disorientation and confusion are not inevitable
parts of aging, but problems linked to that all-important lifestyle factor:
diet.

There is now good dietary information for the two chief conditions
referring to mental decline. On the modest side, there is a condition
called "cognitive impairment" or "cognitive dysfunction." This condi-
tion describes the declining ability to remember and think as well as one
once did. It represents a continuum of disease ranging from cases that
only hint at declining abilities to those that are much more obvious and
easily diagnosed.

Then there are mental dysfunctions that become serious, even life
threatening. These are called dementia, of which there are two main
types: vascular dementia and Alzheimer's disease. Vascular dementia is
primarily caused by multiple little strokes resulting from broken blood
vessels in the brain. It is common for elderly people to have "silent"
strokes in their later years. A stroke is considered silent if it goes un-
detected and undiagnosed. Each little stroke incapacitates part of the
brain. The other type of dementia, Alzheimer's, occurs when a protein
substance called beta-amyloid accumulates in critical areas of the brain
as a plaque, rather like the cholesterol-laden plaque that builds up in
cardiovascular diseases.

Alzheimer's is surprisingly common. It is said that 1% of people at
age sixty-five have evidence of Alzheimer's, a figure that doubles every
five years thereafter. 48 I suppose this is why we blandly accept "senility"
as part of the aging process.

It has been estimated that 10-12% of individuals with mild cognitive
impairment progress to the more serious types of dementia, whereas
only 1-2% of individuals without cognitive impairment acquire these

WIDE-RANGING EFFECTS: BONE, KIDNEY, EYE, BRAIN DISEASES 219

diseases. 49, 50 This means that people with cognitive impairment have
about a tenfold risk of Alzheimer's.

Not only does cognitive impairment often lead to more serious de-
mentia, it is also associated with cardiovascular disease, 51-53 stroke 54 and
adult-onset Type 2 diabetes. 55,55 All of these diseases cluster in the same
populations, oftentimes in the same people. This clustering means that
they share some of the same risk factors. Hypertension (high blood
pressure) is one factor 51 ' 57 58 ; another is high blood cholesterol. 53 Both
of these, of course, can be controlled by diet.

A third risk factor is the amount of those nasty free radicals, which
wreak havoc on brain function in our later years. Because free radical
damage is so important to the process of cognitive dysfunction and
dementia, researchers believe that consuming dietary antioxidants can
shield our brains from this damage, as in other diseases. Animal-based
foods lack antioxidant shields and tend to activate free radical produc-
tion and cell damage, while plant-based foods, with their abundant an-
tioxidants, tend to prevent such damage. It's the same dietary cause and
effect that we saw with macular degeneration.

Of course, genetics plays a role, and specific genes have been identi-
fied that may increase the risk of cognitive decline. 52 But environmental
factors also play a key role, most probably the dominant one.

In a recent study, it was found that Japanese American men living
in Hawaii had a higher rate of Alzheimer's disease than Japanese living
in Japan. 59 Another study found that native Africans had significantly
lower rates of dementia and Alzheimer's than African Americans in In-
diana. 60 Both of these findings clearly support the idea that environment
plays an important role in cognitive disorders.

Worldwide, the prevalence patterns of cognitive disorders appear to
be similar to other Western diseases. Rates of Alzheimer's are low in less
developed areas. 61 A recent study compared Alzheimer's rates to dietary
variables across eleven different countries and found that populations
with a high fat intake and low cereal and grain intake had higher rates
of the disease. 62 63

We seem to be on to something. Clearly diet has an important voice
in determining how well we think in our later years. But what exactly
is good for us?

With regard to the more mild cognitive impairment condition, recent
research has shown that high vitamin E levels in the blood are related
to less memory loss. 64 Less memory loss also is associated with higher

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levels of vitamin C and selenium, both of which reduce free radical ac-
tivity. 65 Vitamins E and C are antioxidants found almost exclusively in
plant foods, while selenium is found in both animal- and plant-based
foods.

In a study of 260 elderly people aged sixty-five to ninety years, it was
reported that: "A diet with less fat, saturated fat and cholesterol, and
more carbohydrate, fiber, vitamins (especially folate, vitamins C and E
and beta-carotenes) and minerals (iron and zinc) may be advisable not
only to improve the general health of the elderly but also to improve
cognitive function." 66 This conclusion advocates plant-based foods and
condemns animal-based foods for optimal brain function. Yet another
study on several hundred older people found that scores on mental tests
were higher among those people who consumed the most vitamin C
and beta-carotene. 67 Other studies have also found that a low level of
vitamin C in the blood is linked to poorer cognitive performance in old
age, 68, 69 and some have found that B vitamins, 69 including beta-caro-
tene, 70 are linked to better cognitive function.

The seven studies mentioned above all show that one or more nutri-
ents found almost exclusively in plants are associated with a lower risk
of cognitive decline in old age. Experimental animal studies have not
only confirmed that plant foods are good for the brain, but they show
the mechanisms by which these foods work. 71, 72 Although there are
important variations in some of these study findings — for example, one
study only finds an association for vitamin C, and another only finds
an association for beta-carotene and not vitamin C — we shouldn't miss
the forest by focusing on one or two trees. No study has ever found that
consuming more dietary antioxidants increases memory loss. When as-
sociations are observed, it is always the other way around. Furthermore,
the association appears to be significant, although more substantial re-
search must be done before we can know exactly how much cognitive
impairment is due to diet.

What about the more serious dementia caused by strokes (vascular
dementia) and Alzheimer's? How does diet affect these diseases? The de-
mentia that is caused by the same vascular problems that lead to stroke
is clearly affected by diet. In a publication from the famous Framingham
Study, researchers conclude that for every three additional servings of
fruits and vegetables a day, the risk of stroke will be reduced by 22%. 73
Three servings of fruits and vegetables is less than you might think. The
following examples count as one serving in this study: 1/2 cup peaches,

WIDE-RANGING EFFECTS: BONE, KIDNEY, EYE, BRAIN DISEASES 221

1/4 cup tomato sauce, 1/2 cup broccoli or one potato. 73 Haifa cup is not
much food. In fact, the men in this study who consumed the most fruits
and vegetables consumed as many as nineteen servings a day. If every
three servings lower the risk by 22%, the benefits can add up fast (risk
reduction approaches but cannot exceed 100%).

This study provides evidence that the health of the arteries and ves-
sels that transport blood to and from your brain is dependent on how
well you eat. By extension, it is logical to assume that eating fruits and
vegetables will protect against dementia caused by poor vascular health.
Research again seems to prove the point. Scientists conducted mental
health exams and assessed food intake for over 5,000 older people and
monitored their health for over two years. They found that the people
who consumed the most total fat and saturated fat had the highest risk
of dementia due to vascular problems. 74

Alzheimer's disease is also related to diet and is often found in con-
junction with heart disease, 53 which suggests that they share the same
causes. We know what causes heart disease, and we know what offers
the best hope of reversing heart disease: diet. Experimental animal stud-
ies have convincingly shown that a high-cholesterol diet will promote
the production of the beta-amyloid common to Alzheimer's. ,3 In con-
firming these experimental animal results, a study of more than 5,000
people found that greater dietary fat and cholesterol intake tended to
increase the risk of Alzheimer's disease specifically 75 and all dementia
in general. 74

In another study on Alzheimer's, 76 the risk of getting the disease was
3.3 times greater among people whose blood folic acid levels were in
the lowest one-third range and 4.5 times greater when blood homo-
cysteine levels were in the highest one-third. What are folic acid and
homocysteine? Folic acid is a compound derived exclusively from
plant-based foods such as green and leafy vegetables. Homocysteine
is an amino acid that is derived primarily from animal protein. 77 This
study found that it was desirable to maintain low blood homocysteine
and high blood folic acid. In other words, the combination of a diet high
in animal-based foods and low in plant-based foods raises the risk of
Alzheimer's disease. 78

Mild cognitive impairment, the stuff jokes are made of, still permits
the afflicted person to maintain an independent, functional life, but
dementia and Alzheimer's are tragic, imposing almost impossibly heavy
burdens on victims and their loved ones. Across this spectrum, from

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minor difficulties in keeping your thoughts in order to serious degen-
eration, the food you eat can drastically affect the likelihood of mental
decline.

The diseases I've covered in this chapter take a heavy toll on most of
us in our later years, even though they may not be fatal. Because they
are not usually fatal, many people afflicted with these illnesses still live
a long life. Their quality of life, however, deteriorates steadily, until the
illness renders them largely dependent on others and unable to function
in most capacities.

I've talked to so many people who say, "I may not live as long as
you health nuts, but I sure am going to enjoy the time I have by eating
steaks whenever I want, smoking if I so choose and doing anything else
that I want." I grew up with these people, went to school with these
people and made great friends with these people. Not long ago, one of
my best friends suffered a difficult surgery for cancer and spent his last
years paralyzed in a nursing home. During the many visits I made to the
nursing home, I never failed to come away with a deep appreciation for
the health I still possess in my old age. It was not uncommon for me to
go to the nursing home to visit my friend and hear that one of the new
patients in the home was someone whom my friend and I knew from
our earlier days. Too often, they had Alzheimer's and were housed in a
special section of the facility.

The enjoyment of life, especially the second half of life, is greatly
compromised if we can't see, if we can't think, if our kidneys don't work
or if our bones are broken or fragile. I, for one, hope that I am able to
fully enjoy not only the time in the present, but also the time in the fu-
ture, with good health and independence.

Part III

THE GOOD NUTRITION GUIDE

I was in a restaurant recently, looking at the menu, when I noticed a very
peculiar "low-carb" meal option: a massive plate of pasta topped with veg-
etables, otherwise known as pasta primavera. The vast majority of calories
in the meal clearly came from carbohydrates. How could it be "low-carb"?
Was it a misprint? I didn't think so. At various other times I've noted
that salads, breads and even cinnamon buns are labeled "low-carb," even
though their ingredient lists demonstrate that, in fact, the bulk of calories
are provided by carbohydrates. What's going on?

This "carb" mania is largely the result of the late Dr. Atkins and his
dietary message. But recently Dr. Atkins' New Diet Revolution has been
toppled and replaced by The South Beach Diet as the king of the diet
books. The South Beach Diet is pitched as being more moderate, easier
to follow and safer than Atkins, but from what I can tell, the weight-loss
"wolf has just put on a different set of sheep's clothing. Both of the di-
ets are divided into three stages, both diets severely limit carbohydrate
intake during the first phase, and both diets are heavily based on meat,
dairy and eggs. The South Beach Diet, for example, prohibits bread,
rice, potatoes, pasta, baked goods, sugar and even fruit during the first
two weeks. After that, you can be weaned back onto carbohydrates until
you are eating what appears to me to be a fairly typical American diet.
Perhaps this is why The South Beach Diet is such a hot seller. According
to The South Beach Diet Web site, Newsweek wrote, "the real value of
the book is its sound nutritional advice. It retains the best part of the
Atkins regime — meat — while losing the tenet that all carbs should be
avoided." 1

223

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THE CHINA STUDY

Who at Newsweek reviewed the literature to know whether this is
sound nutritional advice or not? And if you have the Atkins Diet plus
some "carbs," how different is this diet from the standard American
diet, the toxic diet that has been shown to make us fat, give us heart
disease, destroy our kidneys, make us blind and lead us to Alzheimer's,
cancer and a host of other medical problems?

These are merely examples of the current state of nutrition aware-
ness in the United States. Every day I am reminded that Americans are
drowning in a flood of horrible nutrition information. I remember the
adage told several decades ago: Americans love hogwash. Another one:
Americans love to hear good things about their bad habits. It would ap-
pear from a quick glance that these two sayings are true. Or are they?

I have more faith in the average American. It's not true that Ameri-
cans love hogwash — it's that hogwash inundates Americans, whether
they want it or not! I know that some Americans want the truth, and
just haven't been able to find it because it is drowned out by the hog-
wash. Very little of the nutrition information that makes it to the public
consciousness is soundly based in science, and we pay a grave price.
One day olive oil is terrible, the next it is heart healthy. One day eggs
will clog your arteries, the next they are a good source of protein. One
day potatoes and rice are great, the next they are the gravest threats to
your weight you will ever face.

At the beginning of the book I said my goal was to redefine how we
think of nutrition information — eliminate confusion, make health sim-
ple and base my claims on the evidence generated by peer-reviewed nu-
trition research published in peer-reviewed, professional publications.
So far, you have seen a broad sample — and it's only a sample — of that
evidence. You have seen that there is overwhelming scientific support
for one, simple optimal diet — a whole foods, plant-based diet.

I want to condense the nutritional lessons learned from this broad
range of evidence and from my experiences over the past forty-plus
years into a simple guide to good nutrition. I have whittled my knowl-
edge down to several core principles, principles that will illuminate how
nutrition and health truly operate. Furthermore, I have translated the
science into dietary recommendations that you can begin to incorporate
into your own life. Not only will you gain a new understanding of nutri-
tion and health, but you will also see exactly which foods you should
eat and which foods you should avoid. What you decide to do with this
information is up to you, but you can at least know that you, as a reader
and a person, have finally been told something other than hogwash.

Eating Right: Eight Principles
of Food and Health

The benefits of a healthy lifestyle are enormous. I want you to know
that you can:

• live longer

• look and feel younger

• have more energy

• lose weight

• lower your blood cholesterol

• prevent and even reverse heart disease

• lower your risk of prostate, breast and other cancers

• preserve your eyesight in your later years

• prevent and treat diabetes

• avoid surgery in many instances

• vastly decrease the need for pharmaceutical drugs

• keep your bones strong

• avoid impotence

• avoid stroke

• prevent kidney stones

• keep your baby from getting Type 1 diabetes

• alleviate constipation

• lower your blood pressure

• avoid Alzheimer's

225

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• beat arthritis

• and more . . .

These are only some of the benefits, and all of them can be yours. The
price? Simply changing your diet. I don't know that it has ever been so
easy or so relatively effortless to achieve such profound benefits.

I have given you a sampling of the evidence and told you the journey
that I have taken to come to my conclusions. Now I want to summarize
the lessons about food, health and disease that I have learned along the
way in the following eight principles. These principles should inform the
way we do science, the way we treat the sick, the way we feed ourselves,
the way we think about health and the way we perceive the world.

PRINCIPLE #1

Nutrition represents the combined activities of
countless food substances. The whole is
greater than the sum of its parts.

To illustrate this principle I only need to take you through the biochem-
ical perspective of a meal. Let's say you prepare saut^ed spinach with
ginger and whole grain ravioli shells stuffed with butternut squash and
spices, topped with a walnut tomato sauce.

The spinach alone is a cornucopia of various chemical components.
Chart 11.1 is only a partial list of what you might find in your mouth
after a bite of spinach.

As you can see, you've just introduced a bundle of nutrients into your
body. In addition to this extremely complex mix, when you take a bite
of that ravioli with its tomato sauce and squash filling, you get thou-
sands and thousands of additional chemicals, all connected in different
ways in each different food — truly a biochemical bonanza.

As soon as this food hits your saliva, your body begins working its
magic, and the process of digestion starts. Each of these food chemicals
interacts with the other food chemicals and your body's chemicals in
very specific ways. It is an infinitely complex process, and it is literally
impossible to understand precisely how each chemical interacts with
every other chemical. We will never discover exactly how it all fits to-
gether.

EATING RIGHT: EIGHT PRINCIPLES OF FOOD AND HEALTH 227

CHART 11.1: NUTRIENTS IN SPINACH

Macronutrients

Water

Fat (many kinds)

Calories

Carbohydrate

Protein (many kinds)

Fiber

Minerals

Calcium

Sodium

Iron

Zinc

Magnesium

Copper

Phosphorus

Manganese

Potassium

Selenium

Vitamins

C (Ascorbic Acid)

B-6 (Pyridoxine)

B-1 (Thiamin)

Folate

FJ-2 (Riboflavin)

A (as carotenoids)

B-3 (Niacin)

E (tocopherols]

Pantothenic acid

Fatty Acids

14:0 (Myristic acid)

18:1 (Oleic acid)

16:0 (Palmitic acid)

20:1 (Eicosenoic acid)

18:0 (Stearic acid)

1 8:2 (Linoleic acid)

16:1 (Palmitoleic acid)

1 8:3 (Linolenic acid)

Amino acids

Tryptophan

Valine

Threonine

Arginine

Isoleucine

Histidine

Leucine

Alanine

Lysine

Aspartic acid

Methionine

Glutamic acid

Cystine

Glycine

Phenylalanine

Proline

Tyrosine

Serine

Phytosterols (many kinds)

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The main message I'm trying to get across is this: the chemicals
we get from the foods we eat are engaged in a series of reactions that
work in concert to produce good health. These chemicals are carefully
orchestrated by intricate controls within our cells and all through our
bodies, and these controls decide what nutrient goes where, how much
of each nutrient is needed and when each reaction takes place.

Our bodies have evolved with this infinitely complex network of
reactions in order to derive maximal benefit from whole foods, as they
appear in nature. The misguided may trumpet the virtues of one specific
nutrient or chemical, but this thinking is too simplistic. Our bodies
have learned how to benefit from the chemicals in food as they are pack-
aged together, discarding some and using others as they see fit. I cannot
stress this enough, as it is the foundation of understanding what good
nutrition means.

PRINCIPLE #2

Vitamin supplements are not
a panacea for good health.

Because nutrition operates as an infinitely complex biochemical system
involving thousands of chemicals and thousands of effects on your
health, it makes little or no sense that isolated nutrients taken as sup-
plements can substitute for whole foods. Supplements will not lead to
long-lasting health and may cause unforeseen side effects. Furthermore,
for those relying on supplements, beneficial and sustained diet change
is postponed. The dangers of a Western diet cannot be overcome by
consuming nutrient pills.

As 1 have watched the interest in nutrient supplements explode over
the past twenty to thirty years, it has become abundantly clear why
such a huge nutrient supplement industry has emerged. Huge profits
are an excellent incentive, and new government regulations have paved
the way for an expanded market. Furthermore, consumers want to
continue eating their customary foods, and popping a few supplements
makes people feel better about the potentially adverse health effects
caused by their diet. Embracing supplements means the media can tell
people what they want to hear and doctors have something to offer their
patients. As a result, a multibillion-dollar supplement industry is now

EATING RIGHT: EIGHT PRINCIPLES OF FOOD AND HEALTH

229

part of our nutritional landscape, and the majority of consumers have
been duped into believing that they are buying health. This was the late
Dr. Atkins's formula. He advocated a high-protein, high-fat diet — sacri-
ficing long-term health for short-term gain — and then advocated taking
his supplements to address what he called, in his own words, the "com-
mon dieters' problems" including constipation, sugar cravings, hunger,
fluid retention, fatigue, nervousness and insomnia. 1

This strategy of gaining and maintaining health with nutrient supple-
ments, however, started to unravel in 1994-1996 with the large-scale
investigation of the effects of beta-carotene (a precursor to vitamin A)
supplements on lung cancer and other diseases. 2, 3 After four to eight
years of supplement use, lung cancer had not decreased as expected;
it had increased! No benefit was found from vitamins A and E for the
prevention of heart disease either.

Since then, a large number of additional trials costing hundreds of
millions of dollars have been conducted to determine if vitamins A, C
and E prevent heart disease and cancer. Recently two major reviews of
these trials were published. 4, 5 The researchers, in their words, "could
not determine the balance of benefits and harms of routine use of
supplements of vitamins A, C or E; multivitamins with folic acid; or
antioxidant combinations for the prevention of cancer or cardiovascular
disease." 4 Indeed, they even recommended against the use of beta-caro-
tene supplements.

It is not that these nutrients aren't important. They are — but only
when consumed as food, not as supplements. Isolating nutrients and
trying to get benefits equal to those of whole foods reveals an ignorance
of how nutrition operates in the body. A recent special article in the New
York Times 6 documents this failure of nutrient supplements to provide
any proven health benefit. As time passes, I am confident that we will
continue to "discover" that relying on the use of isolated nutrient sup-
plements to maintain health, while consuming the usual Western diet,
is not only a waste of money but is also potentially dangerous.

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PRINCIPLE #3

There are virtually no nutrients in animal-based foods
that are not better provided by plants.

Overall, it is fair to say that any plant-based food has many more simi-
larities in terms of nutrient compositions to other plant-based foods
than it does to animal-based foods. The same is true the other way
around; all animal-based foods are more like other animal-based foods
than they are to plant-based foods. For example, even though fish is
significantly different from beef, fish has many more similarities to beef
than it has to rice. Even the foods that are "exceptions" to these rules,
such as nuts, seeds and processed low-fat animal products, remain in
distinct plant and animal "nutrient" groups.

Eating animals is a markedly different nutritional experience from
eating plants. The amounts and kinds of nutrients in these two types
of foods, shown in Chart 11.2, 7 ' 8 - 9 illustrate these striking nutritional
differences.

CHART 1 1.2: NUTRIENT COMPOSITION OF PLANT AND
ANIMAL-BASED FOODS (PER 500 CALORIES OF ENERGY)

Nutrient

Plant-Based Foods*

Animal-Based
Foods**

Cholesterol (mg)

137

Fat (g)

Protein (g)

Beta-carotene (meg)

29,919

Dietary Fiber (g)

Vitamin C (mg)

293

Folate (meg)

1 168

Vitamin E (mg_ATE)

1 1

0.5

Iron (mg)

Magnesium (mg)

548

Calcium (mg)

545

252

* Equal parts of tomatoes, spinach, lima beans, peas, potatoes
** Equal parts of beef, pork, chicken, whole milk

EATING RIGHT: EIGHT PRINCIPLES OF FOOD AND HEALTH

231

As you can see, plant foods have dramatically more antioxidants,
fiber and minerals than animal foods. In fact, animal foods are almost
completely devoid of several of these nutrients. Animal foods, on the
other hand, have much more cholesterol and fat. They also have slightly
more protein than plant foods, along with more B ]2 and vitamin D, al-
though the vitamin D is largely due to artificial fortification in milk.
Of course, there are some exceptions: some nuts and seeds are high in
fat and protein (e.g., peanuts, sesame seeds) while some animal-based
foods are low in fat, usually because they are stripped of their fat by ar-
tificial processing (e.g., skim milk). But if one looks a little more closely
the fat and the protein of nuts and seeds are different: they are more
healthful than the fat and protein of animal foods. They also are accom-
panied by some interesting antioxidant substances. On the other hand,
processed, low-fat, animal-based foods still have some cholesterol, lots
of protein and very little or no antioxidants and dietary fiber, just like
other animal-based foods. Since nutrients are primarily responsible for
the healthful effects of foods and because of these major differences in
nutrient composition between animal- and plant-based foods, isn't it
therefore reasonable to assume that we should expect to see distinctly
different effects on our bodies depending on which variety of foods we
consume?

By definition, for a food chemical to be an essential nutrient, it must
meet two requirements:

• the chemical is necessary for healthy human functioning

• the chemical must be something our bodies cannot make on their
own, and therefore must be obtained from an outside source

One example of a chemical that is not essential is cholesterol, a com-
ponent of animal-based food that is nonexistent in plant-based food.
While cholesterol is essential for health, our bodies can make all that
we require; so we do not need to consume any in food. Therefore, it is
not an essential nutrient.

There are four nutrients which animal-based foods have that plant-
based foods, for the most part, do not: cholesterol and vitamins A, D
and B ]2 . Three of these are nonessential nutrients. As discussed above,
cholesterol is made by our bodies naturally. Vitamin A can be readily
made by our bodies from beta-carotene, and vitamin D can be readily
made by our bodies simply by exposing our skin to about fifteen min-
utes of sunshine every couple days. Both of these vitamins are toxic if

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they are consumed in high amounts. This is one more indication that it
is better to rely on the vitamin precursors, beta-carotene and sunshine,
so that our bodies can readily control the timing and quantities of vita-
mins A and D that are needed.

Vitamin B 12 is more problematic. Vitamin B 12 is made by microor-
ganisms found in the soil and by microorganisms in the intestines of
animals, including our own. The amount made in our intestines is not
adequately absorbed, so it is recommended that we consume B ]2 in food.
Research has convincingly shown that plants grown in healthy soil that
has a good concentration of vitamin B 12 will readily absorb this nutri-
ent. 10 However, plants grown in "lifeless" soil (non-organic soil) may
be deficient in vitamin B 12 . In the United States, most of our agriculture
takes place on relatively lifeless soil, decimated from years of unnatural
pesticide, herbicide and fertilizer use. So the plants grown in this soil
and sold in our supermarkets lack B 12 . In addition, we live in such a
sanitized world that we rarely come into direct contact with the soil-
borne microorganisms that produce B ]2 . At one point in our history, we
got B [2 from vegetables that hadn't been scoured of all soil. Therefore, it
is not unreasonable to assume that modern Americans who eat highly
cleansed plant products and no animal products are unlikely to get
enough vitamin B 12 .

Though our society's obsession with nutrient supplements seriously
detracts from other, far more important nutrition information, this is
not to say that supplements should always be avoided. It is estimated
that we hold a three-year store of vitamin B 12 in our bodies. If you do
not eat any animal products for three years or more, or are pregnant or
breastfeeding, you should consider taking a small B 12 supplement on
occasion, or going to the doctor annually to check your blood levels
of B vitamins and homocysteine. Likewise, if you never get sunshine
exposure, especially during the winter months, you might want to take
a vitamin D supplement. I would recommend taking the smallest dose
you can find and making more of an effort to get outside.

I call these supplements "separation from nature pills," because a
healthy diet of fresh, organic plant-based foods grown in rich soil and
a lifestyle that regularly takes you outdoors is the best answer to these
issues. Returning to our natural way of life in this small way provides
innumerable other benefits, as well.

EATING RIGHT: EIGHT PRINCIPLES OF FOOD AND HEALTH

233

PRINCIPLE #4

Genes do not determine disease on their own.
Genes function only by being activated, or expressed,
and nutrition plays a critical role in determining which genes,
good and bad, are expressed.

I can safely say that the origin of every single disease is genetic. Our genes
are the code to everything in our bodies, good and bad. Without genes,
there would be no cancer. Without genes, there would be no obesity, dia-
betes or heart disease. And without genes, there would be no life.

This might explain why we are spending hundreds of millions of dol-
lars trying to figure out which gene causes which disease and how we
can silence the dangerous genes. This also explains why some perfectly
healthy young women have had their breasts removed simply because
they were found to carry genes that are linked to breast cancer. This
explains why the bulk of resources in science and health in the past
decade has shifted to genetic research. At Cornell University alone $500
million is being raised to create a "Life Sciences Initiative." This initia-
tive promises to "forever change the way life -science research is con-
ducted and taught at the university." What is one of the main thrusts of
the program? Integrating each scientific discipline into the all-encom-
passing umbrella of genetic research. It is the largest scientific effort in
Cornell's history."

Much of this focus on genes, however, misses a simple but crucial
point: not all genes are fully expressed all the time. If they aren't activat-
ed, or expressed, they remain biochemically dormant. Dormant genes
do not have any effect on our health. This is obvious to most scientists,
and many laypeople, but the significance of this idea is seldom under-
stood. What happens to cause some genes to remain dormant, and oth-
ers to express themselves? The answer: environment, especially diet.

To reuse a previous analogy, it is useful to think of genes as seeds. As
any good gardener knows, seeds will not grow into plants unless they
have nutrient-rich soil, water and sunshine. Neither will genes be ex-
pressed unless they have the proper environment. In our body, nutrition
is the environmental factor that determines the activity of genes. As we
saw in chapter three, the genes that cause cancer were profoundly im-
pacted by the consumption of protein. In my research group, we learned

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that we could turn the bad genes on and off simply by adjusting animal
protein intake.

Furthermore, our China research findings showed that people of
roughly the same ethnic background have hugely varying disease rates.
These are people said to have similar genes, and yet they get differ-
ent diseases depending on their environment. Dozens of studies have
documented that as people migrate, they assume the disease risk of
the country to which they move. They do not change their genes, and
yet they fall prey to diseases and illnesses at rates that are rare in their
homeland population.

Furthermore, we have seen disease rates change over time so drasti-
cally that it is biologically impossible to put the blame on genes. In
twenty-five years, the percentage of our population that is obese has
doubled, from 15% to 30%. In addition, diabetes, heart disease and
many other diseases of affluence were rare until recent history, and our
genetic code simply could not have changed significantly in the past 25,
100 or even 500 years.

So while we can say that genes are crucial to every biological process,
we have some very convincing evidence that gene expression is far more
important, and gene expression is controlled by environment, especially
nutrition.

A further folly of this genetic research is assuming that understanding
our genes is simple. It is not. Recently for example, researchers studied
genetic regulation of weight in a tiny worm species. 12 The scientists
went through 16,757 genes, turning each one off, and observed the ef-
fect on weight. They discovered 417 genes that affect weight. How these
hundreds of genes interact over the long term with each other and their
ever-changing environment to alter weight gain or loss is an incredibly
complex mystery. Goethe once said, "We know accurately only when
we know little; with knowledge doubt increases." 13

Expression of our genetic code represents a universe of biochemical
interactions of almost infinite complexity. This biochemical "universe"
interacts with many different systems, including nutrition, which it-
self represents whole systems of complex biochemistry. With genetic
research, I suspect we are embarking on a massive quest to shortcut
nature only to end up worse off than when we started.

Does all this mean I think that genes don't matter? Of course not. If
you take two Americans living in the same environment and feed them
exactly the same meaty food every day for their entire lives, I would not

EATING RIGHT: EIGHT PRINCIPLES OF FOOD AND HEALTH

235

be surprised if one died of a heart attack at age fifty-four, and the other
died of cancer at the age of eighty. What explains the difference? Genes.
Genes give us our predispositions. We all have different disease risks due
to our different genes. But while we will never know exactly which risks
we are predisposed to, we do know how to control those risks. Regard-
less of our genes, we can all optimize our chances of expressing the right
genes by providing our bodies with the best possible environment — that
is, the best possible nutrition. Even though the two Americans in the
example above succumbed to different diseases at different ages, it is en-
tirely possible that both could have lived many more years with a higher
quality of life if they would have practiced optimal nutrition.

PRINCIPLE #5

Nutrition can substantially control the adverse effects
of noxious chemicals.

Stories of cancer-causing chemicals regularly appear in the press. Acryl-
amide, artificial sweeteners, nitrosamines, nitrites, Alar, heterocyclic amines
and aflatoxin have all been linked to cancer in experimental studies.

There is a widely held perception that cancer is caused by toxic
chemicals that make their way into our bodies in a sinister way. For
example, people often cite health concerns to justify their opposition to
pumping antibiotics and hormones into farm animals. The assumption
is that the meat would be safe to eat if it didn't have those unnatural
chemicals in it. The real danger of the meat, however, is the nutrient im-
balances, regardless of the presence or absence of those nasty chemicals.
Long before modern chemicals were introduced into our food, people
still began to experience more cancer and more heart disease when they
started to eat more animal-based foods.

A great example of a misunderstood "public health concern" regard-
ing chemicals is the lengthy, $30 million investigation of minimally
higher rates of breast cancer in Long Island, New York, referred to in
chapter eight. Here, it seemed that chemical contaminants from certain
industrial sites were creating breast cancer for women who lived nearby.
But this ill-conceived story has proven to have no merit.

Another chemical carcinogen concern surrounds acrylamide, which
is primarily found in processed or fried foods like potato chips. The

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implication is that if we could effectively remove this chemical from
potato chips, they would be safe to eat, even though they continue to
be highly unhealthy processed slices of potatoes drenched with fat and
salt.

So many of us seem to want a scapegoat. We do not want to hear
that our favorite foods are a problem simply because of their nutritional
content.

In chapter three, we saw that the potential effects of anatoxin, a
chemical touted as being highly carcinogenic, could be entirely con-
trolled by nutrition. Even with large doses of anatoxin, rats could be
healthy, active and cancer-free if they were fed low-protein diets. We
also saw how small findings can make big news every time cancer is
mentioned. For example, if experimental animals have an increased
incidence of cancer after gargantuan exposures, the chemical agent is
trumpeted as a cause of cancer, as was the case for NSAR (see chapter
three) and nitrites. However, like genes, the activities of these chemical
carcinogens are primarily controlled by the nutrients that we eat.

So what do these examples tell us? In practical terms, you aren't do-
ing yourself much good by eating organic beef instead of conventional
beef that's been pumped full of chemicals. The organic beef might be
marginally healthier, but I would never say that it was a safe choice.
Both types of beef have a similar nutrient profile.

It is useful to think of this principle in another way: a chronic disease
like cancer takes years to develop. Those chemicals that initiate cancer
are often the ones that make headlines. What does not make headlines,
however, is the fact that the disease process continues long after initia-
tion, and can be accelerated or repressed during its promotion stage by
nutrition. In other words, nutrition primarily determines whether the
disease will ever do its damage.

PRINCIPLE #6

The same nutrition that prevents disease in its early stages
(before diagnosis) can also halt or reverse disease
in its later stages (after diagnosis).

It is worth repeating that chronic diseases take several years to develop.
For example, there is a general thought that breast cancer can be initi-

EATING RIGHT: EIGHT PRINCIPLES OF FOOD AND HEALTH

237

ated in adolescence and not become detectable until after menopause!
So we very well may have lots of middle-aged women walking around with
breast cancer initiated during their teens that will not be detectable until
after menopause. 1 * For many people this translates into the fatalistic no-
tion that little can be done later in life. Does this mean that these wom-
en should start smoking and eating more chicken-fried steak because
they're doomed anyway? What do we do, given that many of us may
already have an initiated chronic disease lurking in our bodies, waiting
to explode decades from now?

As we saw in chapter three, cancer that is already initiated and grow-
ing in experimental animals can be slowed, halted or even reversed by
good nutrition. Luckily for us, the same good nutrition maximizes health
at every stage of a disease. In humans, we have seen research findings
showing that a whole foods, plant-based diet reverses advanced heart
disease, helps obese people lose weight and helps diabetics get off their
medication and return to a more normal, pre-diabetes life. Research has
also shown that advanced melanoma, the deadly form of skin cancer,
might be attenuated or reversed by lifestyle changes. 15

Some diseases, of course, appear to be irreversible. The autoimmune
diseases are perhaps most frightening because once the body turns
against itself, it may become unstoppable. And yet, amazingly, even
some of these diseases may be slowed or attenuated by diet. Recall the
research showing that even Type 1 diabetics can lower their medication
requirements by eating the right food. Evidence also shows that rheu-
matoid arthritis can be slowed by diet, 16 as can multiple sclerosis. 17 ' 18

I believe that an ounce of prevention does equal a pound of cure, and
the earlier in life good foods are eaten, the better one's health will be.
But for those who already face the burden of disease, we must not forget
that nutrition still can play a vital role.

PRINCIPLE #7

Nutrition that is truly beneficial for one chronic disease
will support health across the board.

When I was trying to get this book published, I had a meeting with an
editor at a major publishing house, and described to her my intent to
create disease-specific chapters that related diet to specific ailments or

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groups of ailments. The editor asked, in effect, "Can you make specific
diet plans for each disease, so that every chapter doesn't have the same
recommendations?" In other words, could I tell people to eat a specific
way for heart disease and a different way for diabetes? The implication,
of course, was that the same eating plan for multiple diseases simply
wasn't catchy enough, wasn't sufficiently "marketable."

Although this might be good marketing, it is not good science. As
I have come to understand more about the biochemical processes of
various diseases, I have also come to see how these diseases have much
in common. Because of these impressive commonalities, it only makes
sense that the same good nutrition will generate health and prevent
diseases across the board. Even if a whole foods, plant-based diet is more
effective at treating heart disease than brain cancer, you can be sure that
this diet will not promote one disease while it stops another. It will nev-
er be "bad" for you. This one good diet can only help across the board.

So I'm afraid I don't have a different, catchy formula for each disease.
I only have one dietary prescription. But rather than be forlorn about its
effect on my book sales, I'd prefer to remain excited about telling you
how simple food and health really is. It is a chance to clear away much
of the incredible public confusion. Quite simply, you can maximize health
for diseases across the board with one simple diet.

PRINCIPLE #8

Good nutrition creates health in all areas of our existence.
All parts are interconnected.

Much has been made of "holistic" health in recent times. This concept
can mean a variety of things to different people. Many people lump all
of the "alternative" medicines and activities into this concept, so holis-
tic health comes to mean acupressure, acupuncture, herbal medicines,
meditation, vitamin supplements, chiropractic care, yoga, aromathera-
py, Feng Shui, massage and even sound therapy.

Conceptually, I believe in holistic health, but not as a catchphrase for
every unconventional and oftentimes unproven medicine around. Food
and nutrition, for example, are of primary importance to our health.
The process of eating is perhaps the most intimate encounter we have
with our world; it is a process in which what we eat becomes part of

EATING RIGHT: EIGHT PRINCIPLES OF FOOD AND HEALTH 239

our body. But other experiences also are important, such as physical
activity, emotional and mental health and the well-being of our environ-
ment. Incorporating these various spheres into our concept of health is
important because they are all interconnected. Indeed, this is a holistic
concept.

These expanding interconnections became apparent to me through
experimentation with animals. The rats fed the low-protein diets were
not only spared liver cancer, but they also had lower blood cholesterol,
noticeably more energy and voluntarily exercised twice as much as the
high-protein rats. The evidence regarding increased energy levels was
supported by an enormous amount of anecdotal evidence 1 have en-
countered over the years: people have more energy when they eat well.
This synergy between nutrition and physical activity is extremely im-
portant, and is evidence that these two parts of life are not isolated from
each other. Good nutrition and regular exercise combine to offer more
health per person than the sum of each part alone.

We also know that physical activity has an effect on emotional and
mental well-being. Much has been said about the effect physical activity
has on various chemicals in our bodies, which in turn affect our moods
and our concentration. And experiencing the rewards of feeling better
emotionally and being more mentally alert provides the confidence and
motivation to treat ourselves to optimal nutrition, which reinforces the
entire cycle. Those who feel good about themselves are more likely to
respect their health by practicing good nutrition.

Sometimes people try to play these different parts of their lives
against each other. People wonder if they can erase bad eating habits
by being a runner. The answer to this is no. The benefits and risks of
diet are crucially important, and more sizable, than the benefits and
risks of other activities. Besides, why would anyone want to try and bal-
ance benefits and risks when they could have all the benefits, working
together? People also wonder whether a perceived health benefit is be-
cause of the exercise or because of a good diet. In the end, that's simply
an academic question. The fact is that these two spheres of our lives
are intimately interconnected, and what's important is that it all works
together to promote or derail health.

Furthermore, it turns out that if we eat the way that promotes the
best health for ourselves, we promote the best health for the planet.
By eating a whole foods, plant-based diet, we use less water, less land,
fewer resources and produce less pollution and less suffering for our

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farm animals. John Robbins has done more than any other person to
bring this issue to the front of American consciousness, and I strongly
recommend reading his most recent book, The Food Revolution.

Our food choices have an incredible impact not only on our metabo-
lism, but also on the initiation, promotion and even reversal of disease,
on our energy, on our physical activity, on our emotional and mental
well-being and on our world environment. AH oj these seemingly sepa-
rate spheres are intimately interconnected.

I have mentioned the wisdom of nature at various points in this
book, and I have come to see the power of the workings of the natural
world. It is a wondrous web of health, from molecules, to people, to
other animals, to forests, to oceans, to the air we breathe. This is nature
at work, from the microscopic to the macroscopic.

WHO CARES, ANYWAY?

The principles outlined in this chapter began, for me, with a narrowly
focused question on diet and cancer in rats, then grew into an ever-ex-
panding universe of questions about human and societal health around
the world. In large measure, the principles in this chapter are the an-
swers to the far-reaching questions that I could not help but ask during
my career.

The applicability of these principles should not be underestimated.
Most importantly, they can help to reduce public confusion regarding
food and health. The latest fads, the newest headlines and the most re-
cent study results are put into a useful context. We need not leap from
our seats every time a chemical is called a carcinogen, every time a new
diet book hits the shelf or every time a headline screams about solving
disease through genetic research.

Simply put, we can relax. We can take a much-needed deep breath
and sit back. Moreover, we can do science more intelligently and ask
better questions because we have a sound framework relating nutrition
to health. In effect, we can interpret new findings with a broader context
in mind. With these newly interpreted findings, we can enrich or modify
our original framework and invest our money and resources where they
matter to increase our society's health. The benefits of understanding
these principles are wide-ranging and profound for individuals, societ-
ies, our fellow animals and our planet.

How to Eat

When my youngest son and collaborator on this book, Tom, was thirteen
years old, our family was in the final stages of a slow shift to becoming
vegetarian. One Sunday morning, Tom came home from a sleepover at a
close friend's house and told us a story I still remember.

The night before, Tom was being grilled, in a friendly way, on his
eating habits. The sister of Tom's friend had asked him, rather incredu-
lously, "You don't eat meat?" My son had never justified his eating hab-
its; he had just gotten used to eating what was on the dinner table. As a
consequence, Tom was not practiced at answering such a question. So
he simply answered, "No, I don't," without offering any explanations.

The girl probed a bit more, "So what do you eat?" My son answered,
with a few shrugs, "I guess just . . . plants." She said, "Oh," and that was
the end of that.

The reason I enjoy this story is because my son's response, "plants,"
was so simple. It was a truthful answer, but couched in an entirely un-
traditional manner. When someone asks for the glazed ham across the
table, she doesn't say, "Pass the flesh of the pig's butt, please," and when
someone tells his children to finish their peas and carrots, he doesn't
say, "Finish your plants." But since my family and I changed our eating
habits, I've come to enjoy thinking of food as either plants or animals.
It fits well into my philosophy of keeping the information on food and
health as simple as possible.

Food and health are anything but simple in our country. I often mar-
vel at the complexity of various weight-loss plans. Although the writers

24 1

242

THE CHINA STUDY

always advertise their plan's ease of use, in reality it's never easy Follow-
ers of these diets have to count calories, points, servings or nutrients or
eat specific amounts of certain foods based on specific, mathematical
ratios. There are tools to be used, supplements to be taken and work-
sheets to be completed. It is no wonder that dieting seldom succeeds.

Eating should be an enjoyable and worry-free experience, and
shouldn't rely on deprivation. Keeping it simple is essential if we are to
enjoy our food.

One of the most fortunate findings from the mountain of nutritional
research I've encountered is that good food and good health is simple. The
biology of the relationship of food and health is exceptionally complex,
but the message is still simple. The recommendations coming from the
published literature are so simple that I can state them in one sentence:
eat a whole foods, plant-based diet, while minimizing the consumption of
refined foods, added salt and added fats. (See table on page 243.)

SUPPLEMENTS

Daily supplements of vitamin B 12 , and perhaps vitamin D for people
who spend most of their time indoors and/or live in the northern cli-
mates are encouraged. For vitamin D, you shouldn't exceed RDA rec-
ommendations.

That's it. That's the diet science has found to be consistent with the
greatest health and the lowest incidence of heart disease, cancer, obesity
and many other Western diseases.

WHAT DOES MINIMIZE MEAN?
SHOULD YOU ELIMINATE MEAT COMPLETELY?

The findings from the China Study indicate that the lower the percent-
age of animal-based foods that are consumed, the greater the health
benefits — even when that percentage declines from 10% to 0% of calo-
ries. So it's not unreasonable to assume that the optimum percentage of
animal-based products is zero, at least for anyone with a predisposition
for a degenerative disease.

But this has not been absolutely proven. Certainly it is true that most
of the health benefits are realized at very low but non-zero levels of
animal-based foods.

My advice is to try to eliminate all animal-based products from your
diet, but not obsess over it. If a tasty vegetable soup has a chicken stock
base, or if a hearty loaf of whole wheat bread includes a tiny amount of

HOW TO EAT

243

EAT ALL YOU WANT (WHILE GETTING LOTS OF VARIETY)
OF ANY WHOLE, UNREFINED PLANT-BASED FOOD

General Category

Specific Examples

Fruits

orange, okra, kiwi, red pepper, apple, cucumber, tomato,
avocado, zucchini, blueberries, strawberries, green pep-
per, raspberries, butternut squash, pumpkin, blackberries,
mangoes, eggplant, pear, watermelon, cranberries, acorn
squash, papaya, grapefruit, peach

Vegetables

Flowers

broccoli, cauliflower (not many of the huge variety of edible
flowers are commonly eaten)

Stems and Leaves

spinach, artichokes, kale, lettuce (all varieties), cabbage,
Swiss chard, collard greens, celery, asparagus, mustard
ulceus, uruoseid dUiouTo, Turnip urctiiid, ueci urecrid, uuk
choi, arugula, Belgian endive, basil, cilantro, parsley, rhu-
barb, seaweed

Roots

potatoes (all varieties), beets, carrots, turnips, onions, garlic,
ginger, leeks, radish, rutabaga

Legumes (seed-
bearing nitrogen-
fixing plants)

green beans, soybeans, peas, peanuts, adzuki beans, black

L L 1 1 ll> • L 1 1

beans, black-eye peas, cannellmi beans, garbanzo beans,
kidney beans, lentils, pinto beans, white beans

Mushrooms

white button, baby bella, cremini, Portobello, shiitake, oys-
ter

Nuts

walnuts, almonds, macadamia, pecans, cashew, hazelnut,
pistachio

Whole grains (in
breads, pastas, etc)

wheat, rice, corn, millet, sorghum, rye, oats, barley, teff,
buckwheat, amaranth, quinoa, kamut, spelt

Refined carbohydrates

pastas (except whole grain varieties), white bread, crackers,
sugars and most cakes and pastries

Added vegetable oils

corn oil, peanut oil, olive oil

Fish

salmon, tuna, cod

CSh[^IEhB8SISBSBSSI1

- / - -

Meat

steak, hamburger, lard

Poultry

chicken, turkey

Dairy

cheese, milk, yogurt

Egg

eggs & products with a high egg content (i.e. mayonnaise)

244

THE CHINA STUDY

egg, don't worry about it. These quantities, very likely, are nutritionally
unimportant. Even more importantly, the ability to relax about very
minor quantities of animal-based foods makes applying this diet much
easier — especially when eating out or buying already-prepared foods.

While I recommend that you not worry about small quantities of
animal products in your food, I am not suggesting that you deliberately
plan to incorporate small portions of meat into your daily diet. My rec-
ommendation is that you try to avoid all animal-based products.

There are three excellent reasons to go all the way. First, following
this diet requires a radical shift in your thinking about food. It's more
work to just do it halfway. If you plan for animal-based products, you'll
eat them — and you'll almost certainly eat more than you should. Second,
you'll feel deprived. Instead of viewing your new food habit as being able
to eat all the plant-based food you want, you'll be seeing it in terms of
having to limit yourself, which is not conducive to staying on the diet
long-term.

If your friend had been a smoker all of his or her life and looked to
you for advice, would you tell them to cut down to only two cigarettes
a day, or would you tell them to quit smoking all together? It's in this
way that I'm telling you that moderation, even with the best intentions,
sometimes makes it more difficult to succeed.

CAN YOU DO THIS?

For most Americans, the idea of giving up virtually all meat products —
including beef, chicken, fish, cheese, milk and eggs — seems impossible.
You might as well ask Americans to stop breathing. The whole idea
seems strange, fanatical or fantastic.

This is the biggest obstacle to the adoption of a plant-based diet: most
people who hear about it don't seriously consider it, despite the truly
impressive health benefits.

If you are one of these people — if you are curious about these find-
ings but know in your heart that you will never be able to give up
meat-then I know that no amount of talk will ever convince you to
change your mind.

You have to try it.

Give it one month. You've been eating cheeseburgers your whole life;
a month without them won't kill you.

A month isn't enough time to give you any long-term benefits, but it
is long enough for you to discover four things:

HOW TO EAT

245

1 . There are some great foods you can eat in a plant-based diet that
you otherwise may never have discovered. You may not be eat-
ing everything you want (desire for meat may last longer than a
month), but you will be eating lots of great, delicious foods.

2. It's not all that bad. Some people take to this diet quite quickly
and love it. Many take months to fully adjust to it. But almost
everyone will find that it's a lot easier than they thought.

3. You'll feel better. Even after only a month, most people will feel
better and likely lose some weight, too. Try having your blood
work done both before and after. Odds are, you'll see significant
improvement in even that period of time.

4. Most importantly, you'll discover that it's possible. You may love
the diet, or you may not, but at the very least you'll come away
from your one-month trial knowing that it's possible. You can do
it, if you choose to. All the health benefits discussed in this book
are not just for Tibetan monks and fanatical spartans. You can
have them too. It's your choice.

The first month can be challenging (more on this shortly) , but it gets
much easier after that. And for many, it becomes a great pleasure.

I know this is hard to believe until you experience it for yourself, but
your tastes change when you are on a plant-based diet. You not only
lose your taste for meat, you begin to discover new flavors in much of
your food, flavors that were dulled when you ate a primarily animal-
based diet. A friend of mine once described it as like being dragged to an
independent film when you wanted to go to the latest Hollywood action
flick. You go in muttering, but you discover, to your surprise, that the
film is great — and much more fulfilling than the "shoot 'em up" movie
would have been.

THE TRANSITION

If you take me up on my suggestion of trying a plant-based diet for one
month, there are five main challenges you'll likely face:

• In the first week, you may have some stomach upset as your diges-
tive system adjusts. This is natural; it is nothing to worry about
and doesn't usually last long.

• You'll need to put some time into this. Don't begrudge this time —
heart disease and cancer take time too. Specifically, you'll need to
learn some new recipes, be willing to try new dishes, discover new

246

THE CHINA STUDY

restaurants. You'll need to pay attention to your tastes and come up
with meals that you really enjoy. This is key.

• You'll need to adjust psychologically No matter how full the plate
is, many of us were trained to think that without meat, it's not a
real meal — especially at dinner. You'll need to overcome this preju-
dice.

• You may not be able to go to the same restaurants you used to go
to, and if you can, you certainly won't be able to order the same
things. This takes some adjustment.

• Your friends, family and colleagues may not be supportive. For
whatever reasons, many people will find it threatening that you
are now a vegetarian or vegan. Perhaps it's because, deep down,
they know their diet isn't very healthy and find it threatening that
someone else is able to give up unhealthy eating habits when they
cannot.

I'd also like to offer you a few pieces of advice for your first month:

• In the long term, plant-based eating is cheaper than an animal-
based diet, but as you learn you may spend a little extra money
trying things. Do it. It's worth it.

• Eat well. If you eat out, try lots of restaurants to find some great
vegan dishes. Often, ethnic restaurants not only offer the most op-
tions for plant-based meals, but the unique tastes are exquisite.
Learn what's out there.

• Eat enough. One of your health goals may be to lose weight. That's
fine, and on a plant-based diet you almost certainly will. But don't
hold back — whatever you do, don't go hungry.

• Eat a variety. Mixing it up is important both for getting all the nec-
essary nutrients and for maintaining your interest in the diet.

The bottom line is that you can eat a plant-based diet with great plea-
sure and satisfaction. But making the transition is a challenge. There
are psychological barriers and practical ones. It takes time and effort.
You may not get support from your friends and family But the benefits
are nothing short of miraculous. And you'll be amazed at how easy it
becomes once you form new habits.

Take the one-month challenge. You'll not only do great things for
yourself, you'll be part of the vanguard working toward moving Ameri-
ca into a healthier, leaner future.

HOW TO EAT

247

Glenn is an associate of mine who, until recently, was a dedicated
meat-eater. In fact, he was recently on the Atkins diet, lost some
weight, but dropped off it when his cholesterol went through the
roof. He's forty-two and overweight. I gave him a draft of the man-
uscript for the China Study and he agreed to take the one-month
challenge. Here are a few of his observations:

GLENN'S TIPS

The first week is quite challenging. It's hard to figure out what to eat. I'm
not much of a cook, so I got some recipe books out and tried creating
some vegan dishes. As someone who would swing through McDonald's
or heat up a frozen dinner, I found it annoying to have to cook meals
each evening. At least half of them were a disaster and had to be thrown
out. But over time I found a few that were fantastic. My sister gave me
a recipe for West African peanut stew that was incredible and like noth-
ing I ever tasted. My mom gave me a vegetarian chili recipe that was
great. And I stumbled on a great whole wheat spaghetti dish with lots
of vegetables and a faux meat sauce (made from soy) that was amazing.
I challenge anyone to know that this was a vegan dish. But all of this
does take time.

I'm rediscovering fruit. I've always loved fruit, but for some reason
I don't really eat much of it. Maybe it's not eating meat, but I'm finding
that I'm enjoying fruit more than ever. I now cut up a grapefruit and eat
it as a snack. I really like it! I would have never done that before; I actu-
ally think my tastes are getting more sensitive.

I was avoiding eating out — something I used to do constantly — for
fear of not having a vegan option. But I'm getting more adventurous
now. I've found some new restaurants that have some great vegan side
dishes, including a wonderful local Vietnamese place (I know that most
Vietnamese food isn't strictly vegan, since they use a fish sauce in many
dishes, but for nutritional purposes it's very close). The other day I got
dragged into a pizza place with a large group; there was nothing I could
do, and I was starved. I ordered a cheese-less pizza with lots of veg-
etables. They even made it with a whole wheat crust. I was prepared to
choke it down but actually it was surprisingly good. I've brought that
home a few times since.

I'm finding that cravings for meat products are pretty much gone,
particularly if I don't let myself get hungry. And, honestly, I'm eating

248

THE CHINA STUDY

like a pig. Being overweight, I've always been self-conscious about what
I eat. Now I eat like a madman, and feel virtuous to boot. I can honestly
say I'm enjoying the food I'm eating now a lot more than before, partly
because I'm fussier now in what I eat. I only eat foods I really like.

The first month went by quicker than I thought it would. I've lost
eight pounds and my cholesterol has dropped dramatically. I'm spend-
ing a lot less time on this now, particularly since I've found so many
restaurants I can eat at, plus I cook huge meals and then freeze them.
My freezer is stocked with vegan goodies.

The experiment is over but I stopped thinking of it as an experiment
weeks ago. I can't imagine why I would go back to my old eating pat-
terns.

Part IV

WHY HAVEN'T YOU
HEARD THIS BEFORE?

Often when people hear of scientific information that justifies a radical
shift in diet to plant foods, they can't believe their ears. "If all that you
say is true," they wonder, "why haven't I heard it before? In fact, why
do I usually hear the opposite of what you say: that milk is good for us,
that we need meat to get protein and that cancer and heart disease are
all in the genes?" These are legitimate questions, and the answers are
a crucial part of this story. In order to get to these answers, however, I
believe that it is essential for us to know how information is created and
how it reaches the public consciousness.

As you will come to see, much is governed by the Golden Rule: he
who has the gold makes the rules. There are powerful, influential and
enormously wealthy industries that stand to lose a vast amount of
money if Americans start shifting to a plant-based diet. Their financial
health depends on controlling what the public knows about nutrition
and health. Like any good business enterprise, these industries do ev-
erything in their power to protect their profits and their shareholders.

You might be inclined to think that industry pays scientists under
the table to "cook the data," bribes government officials or conducts
illegal activities. Many people love a sensational story. But the power-
ful interests that maintain the status quo do not usually conduct illegal

249

250

THE CHINA STUDY

business. As far as I know, they do not pay scientists to "cook the data."
They do not bribe elected officials or make sordid underhanded deals.
The situation is much worse.

The entire system — government, science, medicine, industry and
media — promotes profits over health, technology over food and confu-
sion over clarity. Most, but not all, of the confusion about nutrition is
created in legal, fully disclosed ways and is disseminated by unsuspect-
ing, well-intentioned people, whether they are researchers, politicians
or journalists. The most damaging aspect of the system is not sensa-
tional, nor is it likely to create much of a stir upon its discovery. It is a
silent enemy that few people see and understand.

My experiences within the scientific community illustrate how the
entire system generates confusing information and why you haven't
heard the message of this book before. In the following chapters, I have
divided the "system" of problems into the entities of science, govern-
ment, industry and medicine, but, as you will come to see, there are
instances where it is nearly impossible to distinguish science from in-
dustry, government from science or government from industry.

Science— The Dark Side

When I was living in a mountain valley outside of Blacksburg, Virginia,
my family enjoyed visiting a retired farmer down the road, Mr. Kinsey,
who always had a funny story to tell. We used to look forward to eve-
nings listening to his stories on his front porch. One of my favorites was
the great potato bug scam.

He told us of his farm days before pesticides, and recounted that
when a potato crop became infested with potato bugs, the bugs had
to be removed and killed, one by one, by hand. One day, Mr. Kinsey
noticed an advertisement in a farm magazine for a great potato bug
killer, on sale for five dollars. Although five dollars was no small sum
of money in those days, Mr. Kinsey figured the bugs were enough of a
hassle to warrant the investment. A short while later, when he received
the great potato bug killer, he opened the package and found two blocks
of wood and a short list of three instructions:

• Pick up one block of wood.

• Place the potato bug on the flat face of the wood.

• Pick up the second block of wood and press firmly onto the potato bug.

Scams, tricks and outright deception for personal gain are as old as
history itself, and perhaps no discipline in our society has suffered more
from this affliction than the discipline of health. Very few experiences
are as personal and as powerful as those of people who have lost their
health prematurely. Understandably, they are willing to believe and try
just about anything that might help. They are a highly vulnerable group
of consumers.

251

252

THE CHINA STUDY

In the mid-1970s, along came a prime example of a health scam, at
least according to the medical establishment. It concerned an alternative
cancer treatment called Laetrile, a natural compound made largely from
apricot pits. If you had cancer and had been unsuccessfully treated by
your regular doctors here in the United States, you may have considered
heading to Tijuana, Mexico. Washington Post Magazine documented the
story of Sylvia Dutton, a fifty-three-year-old woman from Florida, who
had done just that as a last attempt to thwart a cancer that had already
spread from her ovaries to her lymph system. 1 Friends and fellow
churchgoers had told her and her husband about the Laetrile treatment
and its ability to cure advanced cancer. In the magazine article, 1 Sylvia's
husband said, "There are at least a dozen people in this area who were
told they were going to be dead from cancer who used Laetrile and now
they're out playing tennis."

The catch, however, was that Laetrile was a highly contentious treat-
ment. Some people in the medical establishment argued that animal
studies had repeatedly shown Laetrile to have no effect on tumors. 1
Because of this, the U.S. Food and Drug Administration had decided
to suppress the use of Laetrile, which gave rise to the popular clinics
south of the border. One famous hospital in Tijuana treated "as many
as 20,000 American patients a year." 1 One of those patients was Sylvia
Dutton, for whom Laetrile unfortunately did not work.

But Laetrile was only one of many alternative health products. By the
end of the 1970s, Americans were spending $1 billion a year on vari-
ous supplements and potions that promised magical benefits. 2 These
included pangamic acid, which was touted as a previously undiscovered
vitamin with virtually unlimited powers, various bee concoctions and
other supplement products including garlic and zinc. 2

At the same time in the scientific community, more and more health
information, specifically nutrition information, was being generated
at a furious pace. In 1976, Senator George McGovern had convened
a committee that drafted dietary goals recommending decreased con-
sumption of fatty animal foods and increased consumption of fruits and
vegetables because of their effects on heart disease. The first draft of this
report, linking heart disease and food, caused such an uproar that a ma-
jor revision was required before it was released for publication. In a per-
sonal conversation McGovern told me that he and five other powerful
senators from agricultural states lost their respective elections in 1980
in part because they had dared to take on the animal foods industry.

SCIENCE — THE DARK SIDE

253

At the end of the 1970s, the McGovern report succeeded in prodding
the government to produce its first-ever dietary guidelines, which were
rumored to promote a message similar to that of McGovern's commit-
tee. At about the same time, there were widely publicized government
debates about whether food additives were safe, and whether saccharin
caused cancer.

PLAYING MY PART

In the late 1970s I found myself in the middle of this rapidly changing
environment. By 1975 my program in the Philippines had ended, and
I was well into my experimental laboratory work here in the United
States, after having accepted a full professorship with tenure at Cornell
University. Some of my early work on anatoxin and liver cancer in the
Philippines (chapter two) had garnered widespread interest, and my
subsequent laboratory work investigating nutritional factors, carcino-
gens and cancer (chapter three) was attracting national attention. At
that time, I had one of only two or three laboratories in the country do-
ing basic research on nutrition and cancer. It was a novel endeavor.

From 1978 to 1979 1 took a year-long sabbatical leave from Cornell to
go to the epicenter of national nutritional activity, Bethesda, Maryland.
The organization that I was working with was the Federation of Ameri-
can Societies for Experimental Biology and Medicine, or FASEB. Six in-
dividual research societies made up the federation, representing patholo-
gy, biochemistry, pharmacology, nutrition, immunology and physiology.
The FASEB sponsored the annual joint meetings of all six societies, and
upwards of more than 20,000 scientists attended. I was a member of two
of these societies, nutrition and pharmacology and was particularly ac-
tive in the American Institution of Nutrition (now named the American
Society for Nutritional Sciences). My principle work was to chair, under
contract to the Food and Drug Administration, a committee of scientists
investigating potential hazards of using nutrient supplements.

While there, I also was invited to be on a public affairs committee
that served as liaison between the FASEB and Congress. The commit-
tee's charge was to stay on top of congressional activity and represent
our societies' interests in dealings with lawmakers. We reviewed poli-
cies, budgets and position statements, met with congressional staffs,
and held meetings around big, impressive "boardroom" tables in dis-
tinguished, august meeting rooms. I often got the feeling I was in the
citadel of science.

254

THE CHINA STUDY

As a prerequisite to representing my nutrition society on this pub-
lic affairs committee, I first had to decide, for myself, how nutrition is
best defined. It's a far more difficult question than you may think. We
had scientists who were interested in applied nutrition, which involves
people and communities. We had medical doctors interested in isolated
food compounds as pharmacological drugs and research scientists who
only worked with isolated cells and well-identified chemicals in the
laboratory. We even had people who thought nutrition studies should
focus on livestock as well as people. The concept of nutrition was far
from clear; clarification was critical. The average American's view of nu-
trition was even more varied and confused. Consumers were constantly
being duped by fads, yet remained intensely interested in nutrient
supplements and dietary advice coming from any source, whether that
source was a diet book or a government official.

One day in late spring of 1979, while doing my more routine work, I
got a call from the director of the public affairs office at the FASEB who
coordinated the work of our congressional "liaison" committee.

Ellis informed me that there was yet another new committee being
formed within one of the FASEB Societies, the American Institute of
Nutrition, that might interest me.

"It's being called the Public Nutrition Information Committee," he
told me, "and one of its responsibilities will be to decide what is sound
nutritional advice to give to the public.

"Obviously," he said, "there's a big overlap between what this new
committee wants to do and what we do on the public affairs commit-
tee."

I agreed.

"If you're interested, I would like to have you join this new commit-
tee as a representative of the public affairs office," he said.

The proposal sounded good to me because it was early in my career
and it meant getting a chance to hear the scholarly views of some of
the "big name" nutrition researchers. It also was a committee, accord-
ing to its organizers, that could evolve into a "supreme court" of public
nutrition information. It might serve, for example, to identify nutrition
quackery.

SCIENCE — THE DARK SIDE

255

A BIG SURPRISE

At the time that this new Public Nutrition Information Committee was
being formed, a maelstrom was developing across town at the presti-
gious National Academy of Sciences (NAS). A public dispute was taking
place between the NAS president, Phil Handler, and the internal NAS
Food and Nutrition Board. Handler wanted to bring in a group of distin-
guished scientists from outside of the NAS organization to deliberate on
the subject of diet, nutrition and cancer and to write a report. This did
not please his internal Food and Nutrition Board, which wanted con-
trol over this project. Handler's NAS was being offered funding, from
Congress, to produce a report on a subject that had not been previously
considered in this way.

Within the scientific community it was widely known that the NAS
Food and Nutrition Board was strongly influenced by the meat, dairy
and egg industries. Two of its leaders, Bob Olson and Alf Harper, had
strong connections to these industries. Olson was a well-paid consul-
tant to the egg industry, and Harper acknowledged that 10% of his
income came from offering his services to food companies, including
large dairy corporations. 3

Ultimately Handler, as president of the NAS, went around his Food
and Nutrition Board and arranged for a panel of expert scientists from
outside of his organization to write the 1982 report Diet, Nutrition, and
Cancer.' 1 As it turned out, 1 was one of thirteen scientists chosen to be on
the panel to write the report.

As could be expected, Alf Harper, Bob Olson and their Food and
Nutrition Board colleagues were not happy about losing control of this
landmark report. They knew that the report could greatly influence na-
tional opinion about diet and disease. Mostly, they feared that the great
American diet was going to be challenged, perhaps even called a pos-
sible cause of cancer.

James S. Turner, chairman of a related Consumer Liaison Panel with-
in the NAS, was critical of the Food and Nutrition Board and wrote, "We
can only conclude that the [Food and Nutrition] Board is dominated by
a group of change-resistant scientists who share a rather isolated view
about diet and disease." 3

After being denied control of this promising new report on diet,
nutrition and cancer, the pro-industry Board needed to do some dam-
age control. An alternate group was quickly established elsewhere: the

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new Public Nutrition Information Committee. Who were the leaders of
the new Public Nutrition Information Committee? Bob Olson, Alfred
Harper and Tom Jukes, a long-time industry scientist, each of whom
held a university faculty position. I was initially innocent of the group's
purpose, but by our first meeting in the spring of 1980, 1 had discovered
that, of the eighteen members on that committee, 1 was the only indi-
vidual who did not have ties to the commercial world of food and drug
companies and their coalitions.

This committee was a stacked deck; its members were entrenched in
the status quo. Their professional associations, their friends, the people
they fraternized with, were all pro-industry. They enjoyed the meaty
American diet themselves and were unwilling to consider the possibility
that their views were wrong. In addition, some of them enjoyed hand-
some benefits, including first-class travel expenses and nice consulting
fees, paid by animal foods companies. Although there was nothing il-
legal about any of these activities, it certainly laid bare a serious conflict
of interest that put most of the committee members at odds with the
public interest.

This is analogous to the situation, as it unfolded, surrounding ciga-
rettes and health. When scientific evidence first emerged to show that
cigarettes were dangerous, there were hordes of health professionals
who vigorously defended smoking. For example, the Journal of the
American Medical Association continued to advertise tobacco products,
and many others played their part to staunchly defend tobacco use. In
many cases, these scientists were motivated by understandable caution.
But there were quite a few others, particularly as the evidence against
tobacco mounted, whose motivations were clearly personal bias and
greed.

So there I was, on a committee that was to judge the merit of nutri-
tion information, a committee that was comprised of some of the most
powerful pro-industry scientists. I was the only one not hand-picked by
the industry cronies, as I was there at the behest of the director of the
FASEB public affairs office. At that point in my career, I had not formed
any particularly strong views for or against the standard American diet.
More than anything, I was interested in promoting honest, open de-
bate — something that would immediately put me at odds with this new
organization.

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257

THE FIRST MEETING

From the first moment of the first meeting in April 1980, 1 knew I was
the chicken who had wandered into a fox's den, although I went in with
high hopes and an open, though naive, mind. After all, lots of scien-
tists, myself included, have consulted with companies while working to
maintain an objective mind in the best interest of the public health.

In the second session of our first committee meeting the chairman,
Tom Jukes, passed around a proposed news release, handwritten by
himself, regarding the mission of the committee. In addition to an-
nouncing our formation, the news release listed examples of the kind of
nutrition frauds that our committee intended to expose.

As I scanned the list of so-called frauds, I was stunned to see the
1977 McGovern dietary goals 5 on the list. First drafted in 1976, these
relatively modest goals suggested that less meat and fat consumption
and more fruit and vegetable consumption might prevent heart disease.
In this proposed news release, they were described as nothing more
than simple quackery, just like the widely condemned Laetrile and
pangamic acid preparations. In essence, the recommendation to shift
our eating habits to more fruits and vegetables and whole grains was a
fraud. This was the committee's attempt to demonstrate their ability to
be the supreme arbiter of reliable scientific information!

Having looked forward to my membership on this new committee,
I was shocked to see what was emerging. Although I had no particular
predilection toward any one type of diet at the time, I knew that the
landmark diet, nutrition and cancer panel that I was on at the National
Academy of Sciences would likely recommend something similar to Mc-
Govern's goals, this time citing cancer research instead of heart disease
research. The scientific results with which I was familiar very clearly
seemed to justify the moderate recommendations made by McGovern's
dietary goals committee.

Sitting next to me at our first meeting was Alf Harper, whom I had
held in high esteem since our days at MIT where he was the General
Foods Professor of Nutritional Sciences. Early in the meeting, when
this handwritten proposed news release was passed out to the commit-
tee members, I leaned over to Harper and pointed to the place where
it listed McGovern's dietary goals amongst other common scams and
whispered incredulously, "Do you see this?"

Harper could sense my unease, even disbelief, and so quickly spoke

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up. In a patronizing tone, he said to the group, "There are honorable
people in our society who may not necessarily agree with this list. Per-
haps we should put it on hold." A reluctant discussion ensued, and they
decided to forgo the proposed press release.

With the conclusion of the news release issue, the meeting came to
an end. As far as I was concerned, it was a dubious beginning, at best.

A couple of weeks later, back in upstate New York, I turned on a
morning TV news show and Tom Brokaw appeared on the screen and
started talking about nutrition with Bob Olson, of all people. They were
discussing a recent report that Olson and friends had produced at the
National Academy of Sciences called "Toward Healthful Diets." This
report, which was one of the briefest, most superficial reports on health
ever produced by the NAS, extolled the virtues of the high-fat, high-
meat American diet and basically confirmed that all was well with how
America was eating.

From a scientific point of view, the message was a doozy. I remem-
ber one exchange where Tom Brokaw asked about fast food, and Olson
confidently stated that McDonald's hamburgers were fine. With millions
of viewers watching this "expert" praise the health value of McDonald's
hamburgers, it's no wonder that consumers around the country were
confused. Only a handful of insiders could possibly know that his views
did not even come close to reflecting the best understanding of the sci-
ence at the time.

THE SECOND MEETING

We were back for round two in Atlantic City at our annual meeting in
late spring of 1981. From our correspondence over the past year, the
committee already had an informal agenda in place. First, we were to
establish the proposition that nutrition scams were eroding the public's
trust in the nutrition research community. Second, we needed to pub-
licize the idea that advocating more vegetable and fruit consumption
and less meat and high-fat foods was, itself, a scam. Third, we intended
to position our committee as a permanent, standing organization. Up
to this point, our group had only served in a temporary capacity, as
an exploratory committee. Now it was time to get on with our job of
becoming the permanent, principle source of reliable nutrition informa-
tion in the U.S.

Within the first few days of arriving at the convention, a fellow mem-
ber of the committee, Howard Applebaum, told me of the developing

SCIENCE— THE DARK SIDE

259

gossip. "Did you hear?" he whispered. "Olson's decided that they're go-
ing to reconstitute the committee and you are going to be removed." At
that time, Olson was still serving his one-year term as president of the
parent society the American Institute of Nutrition, and had the power
to do such things.

I remember thinking that this news was neither surprising nor dis-
appointing. I knew I was the black sheep of the committee and had al-
ready stepped out of line at our inaugural meeting the previous year. My
continued involvement in this particular group was going to amount to
nothing more than trying to swim up Niagara Falls. The only reason I
was involved in the first place was because the director of the public af-
fairs office at the FASEB had secured me the spot.

I had thought the first year's committee meeting was dubious, but I
ran into an even more bizarre beginning at that second meeting a year
later, before Olson had the chance to remove me. When the proposal
to become a permanent organization within our society was put forth,
I was the only one to challenge the idea. I expressed concern that this
committee and its activities reeked of McCarthyism, which had no place
in a scientific research society What I was saying made the chair of the
committee intensely angry and physically hostile, and I decided it was
best to just leave the room. I was clearly a threat to everything the com-
mittee members wanted to achieve.

After relating the whole ordeal to the newly-elected incoming presi-
dent of the society, Professor Doris Calloway of UC Berkeley, the com-
mittee was abolished and reformed, with me as the chair. Fortunately, I
persuaded our six-member committee to disband after less than a year,
and the whole sorry affair came to an end.

To stay and "fight the good fight," so to speak, was not an option. It
was early in my career and the awesome power wielded by the seniors in
my society was stark and intellectually brutal. For many of these char-
acters, searching for a truth that promoted public health over the status
quo was not an option. I am absolutely convinced that had I busied
myself with tackling these issues so early in my career, I would not be
writing this book. Research funding and publications would have been
difficult if not impossible to obtain.

Meanwhile, Bob Olson and some of his colleagues turned their at-
tention elsewhere, focusing on a relatively new organization founded
in 1978 called the American Council on Science and Health (ACSH).
Headquartered in New York City, the ACSH bills itself, still today, as a

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"consumer education consortium concerned with issues related to food,
nutrition, chemicals, pharmaceuticals, lifestyle, the environment and
health." The group also claims to be an "independent, nonprofit, tax-ex-
empt organization," 6 but they receive 76% of their funding from corpo-
rations and corporate donors, according to the National Environmental
Trust who cite the Congressional Quarterly's Public Interest Profiles. 7

According to the National Environmental Trust, 7 the ACSH has
claimed, in their reports, that cholesterol is not related to coronary
heart disease, "the unpopularity of food irradiation. . . is not based in
science," "endocrine disruptors" (e.g., PCBs, dioxins, etc.) are not a
human health problem, saccharin is not carcinogenic and implementa-
tion of fossil-fuel restrictions to control global warming should not be
implemented. Searching for a serious critique of the food industry from
the ACSH is like searching for a needle in a haystack. Although I believe
that some of their arguments may have merit, I seriously question their
claim to be an objective broker of "consumer education."

FALLING ON MY PETARD

During the entire experience with the Public Nutrition Information Com-
mittee, I continued to work on the National Academy of Sciences report
on diet, nutrition and cancer, which was released in June 1982. 4 As might
have been expected, when this report was published all hell broke loose.
Being the first such report on diet and cancer, it received extensive public-
ity, fast becoming the most sought-after report in NAS history. It was estab-
lishing high-profile goals for the dietary prevention of cancer which were
very similar to those of the 1976 McGovern Committee report on diet and
heart disease. Principally we were encouraging the consumption of fruits,
vegetables and whole grain cereal products, while decreasing total fat in-
take. The fact that this report was concerned with cancer instead of heart
disease, however, elevated emotions. The stakes were high and getting
higher; cancer incites a far greater fear than heart disease.

Given the stakes, some powerful enemies came out of the woodwork.
Within two weeks, the Council on Agriculture, Science and Technology
(CAST), an influential lobbying group for the livestock-based farming
industry, produced a report summarizing the views of fifty-six "experts"
who were concerned about the effect of our NAS report on the agricul-
ture and food industries. Olson, Jukes, Harper and their like-minded
colleagues on the now defunct Public Nutrition Information Commit-
tee weighed in as experts. Their report was quickly published, then

SCIENCE — THE DARK SIDE

261

placed in the hands of all 535 U.S. congressional members. It was clear
that the CAST was deeply concerned about the possible impact that our
report might have on the public.

The CAST wasn't the only group that stepped up to criticize the
report. In addition, there were the American Meat Institute, National
Broiler Council, National Cattlemen's Association, National Livestock
and Meat Board, National Meat Association, National Milk Producers
Federation, National Pork Producers Council, National Turkey Fed-
eration and United Egg Producers. 3 I wouldn't presume to know how
much cancer research the National Turkey Federation conducts, but I'm
guessing that their criticism of our report was not born out of their de-
sire for truth in science.

It was ironic that I had learned some of my most valuable lessons
growing up on a dairy farm, and yet the work I was doing was portrayed
as being at odds with agricultural interests. Of course, these mammoth
corporate interests were far removed from the farmers I knew growing
up — the hardworking, honest families that maintained small farms, just
big enough to get by comfortably. I often have wondered whether these
Washington agricultural interests truly represent America's great farm-
ing tradition, or whether they only represent agricultural conglomerates
with operations worth tens of millions of dollars.

Alf Harper, who had written a strong letter of support for my first
faculty position after leaving MIT, wrote me a stern personal letter in
which he declared that I had "fallen on [my] own petard." A petard is a
type of bomb or firecracker. Apparently, my involvement in the Public
Nutrition Information Committee and the NAS Diet, Nutrition and Can-
cer report was finally too much for even him to bear.

Times were hot, to be sure. Congressional hearings, in which I testi-
fied, were held on the NAS report itself; People magazine featured me in
a prominent article, and an endless series of news media reports contin-
ued over the next year.

AMERICAN INSTITUTE FOR CANCER RESEARCH

It seemed that for the first time in our history, the government was seri-
ously thinking about what we eat as a means of controlling cancer. This
was fertile territory for doing something new, and something new did
indeed fall into my lap. I was invited to assist a new organization called
the American Institute for Cancer Research (AICR) in Falls Church,
Virginia. The founders of this organization were fund-raisers and had

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learned that it was possible to raise, through mailing campaigns, large
sums of money for cancer research. It seemed that many people were
interested in learning something new about cancer beyond the usual
model of surgery, radiation and cytotoxic drugs.

This budding organization was well aware of our 1982 NAS report 4
that focused on diet and cancer, and so invited me to join them as their
senior science advisor. 1 encouraged them to focus on diet because the
nutrition connection with cancer was becoming an important area of
research, yet was receiving very little, if any, support from the major
funding agencies. 1 especially encouraged them to emphasize whole
foods as a source of nutrition, not nutrient supplements, partly because
this was the message of the NAS report.

As I began to work with the A1CR, two challenges simultaneously
arose. First, the AICR needed to get established as a credible organization
to promote the message and to support research. Second, the NAS recom-
mendations needed to be publicized. Therefore, 1 thought it made sense
for the AICR to help publicize the NAS recommendations. Dr. Sushma
Palmer, executive director of the NAS project, 4 and Harvard professor
Mark Hegsted, who was the key advisor to the McGovern Committee,
agreed to join me in endorsing this AICR project. Simultaneously, the
AICR president, Marilyn Gentry, suggested that the AICR could publish
the NAS report and send free copies to 50,000 physicians in the U.S.
These projects, which seemed to me to be logical, useful and socially
responsible, were also highly successful. The associations we were mak-
ing and the exposure we were generating were aimed at increasing the
public's health. As 1 was quick to find out, however, creating an organiza-
tion focused on diet as a central link in cancer causation was seen as a
threat to a great many people. It was clear that the AlCR's projects were
beginning to hit the mark because of the hostile feedback coming from
the food, medical and drug industries. It seemed that every effort was be-
ing made to discredit them.

I was surprised that government interference was particularly harsh.
National and state attorney general offices questioned the AlCR's status
and its fund-raising procedures. The U.S. Post Office joined in the fray,
questioning whether the AICR could use the mail to spread "junk" in-
formation. We all had our suspicions as to who were encouraging these
government offices to quash the dissemination of this diet and cancer
information. Collectively, these public agencies were making life very
difficult. Why were they attacking a nonprofit organization promoting

SCIENCE— THE DARK SIDE 263

cancer research? It all came down to the fact that the AICR, like the
NAS, was pushing an agenda that connected diet and cancer.

The American Cancer Society became an especially vigorous detrac-
tor. In its eyes, the AICR had two strikes against it: it might compete for
the same funding donors, and it was trying to shift the cancer discus-
sion toward diet. The American Cancer Society had not yet acknowl-
edged that diet and nutrition were connected to cancer. (It wasn't until
many years later in the early 1990s that it developed dietary recom-
mendations to control cancer when the idea was receiving considerable
currency with the public.) It was very much a medically-based organi-
zation invested in the conventional use of drugs, radiation and surgery.
A short while before, the American Cancer Society had contacted our
NAS committee about the possibility of our joining them to produce
dietary recommendations to prevent cancer. As a committee, we de-
clined, although a couple of the people on our committee did offer their
individual services. The American Cancer Society seemed to sense a big
story on the horizon and didn't like the idea that another organization,
the AICR, might get the credit.

MISINFORMATION

It may seem that I am coming down a tad harshly on an organization
that most people regard as purely benevolent, but the American Cancer
Society acted differently behind the scenes than it did in public.

On one occasion, I traveled to an upstate New York town where I
had been invited to give a lecture to the local chapter of the American
Cancer Society, as I had done elsewhere. During my lecture, I showed a
slide that made reference to the new AICR organization. I did not men-
tion my personal association, so the audience was not aware that I was
their senior science advisor.

After the lecture, I took questions and my host asked me, "Do you
know that AICR is an organization of quacks?"

"No," I said, "I don't." I'm afraid I didn't do such a good job of hid-
ing my skepticism of her comment, because she felt obliged to explain,
"That organization is being run by a group of quacks and discredited
doctors. Some of them have even served time in prison."

Prison time? This was news to me !

Again, without revealing my association with the AICR, I asked,
"How do you know that?" She said she saw a memo that had been cir-
culated to local American Cancer Society offices around the country.

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Before leaving, I arranged for her to send me a copy of the memo she
was referring to, and, in a day or so, she did.

The memo had been sent from the office of the national president of
the American Cancer Society, who also was a senior executive of the pres-
tigious Roswell Park Memorial Institute for Cancer Research in Buffalo.
This memo alleged that the scientific "chair" of the organization, without
naming me, was heading up a group of "eight or nine" discredited physi-
cians, several of whom had spent time in prison. It was total fabrication.
I didn't even recognize the names of these discredited physicians and had
no idea how something so vicious could have gotten started.

After snooping around a little more, I discovered the person in the
American Cancer Society office in Buffalo who was responsible for the
memo. I phoned him. Not surprisingly, he was evasive and only said
that he had gotten this information from an unnamed reporter. It was
impossible to trace the original source. The one thing I do know for
sure was that this memo was distributed by the office of the American
Cancer Society's president.

I also learned that the National Dairy Council, a powerful industry
lobbying group, had obtained a copy of the same memo and proceeded
to distribute a notice of its own to its local offices around the country.
The smear campaign against the AICR was widespread. The food, phar-
maceutical and medical industries through and/or parallel to the Ameri-
can Cancer Society and the National Dairy Council were showing their
true colors. Prevention of cancer with low-cost, low-profit plant foods
was not welcomed by the food and pharmaco-medical industries. With
support from a trusting media, their combined power to influence the
public was overwhelming.

PERSONAL CONSEQUENCES

The ending of this story, however, is a happy one. Although the AICR's
first couple of years were turbulent and difficult for me both personally
and professionally, the smear campaigns finally started to wane. No lon-
ger considered "on the fringe," the AICR has now expanded to England
(the World Cancer Research Fund, WCRF, in London) and elsewhere.
For over twenty years now, the AICR has run a program that funds
research and education projects on the link between diet and cancer. I
initially organized and chaired that grant program, and then continued
as the AICR's senior science advisor for several years, in a few different
stints, after its initial founding.

SCIENCE — THE DARK SIDE

265

One more unfortunate affair, however, bears mention. I was informed
by my nutrition society's Board of Directors that two society members
(Bob Olson and Alf Harper) had proposed to have me expelled from the
society, supposedly because of my association with the AICR. It would
have been the first expulsion in the history of the society I had to go to
Washington to be "interviewed" by the president of the society and the
director of nutrition at the FDA. Most of their questions concerned the
AICR.

The whole ordeal proved stranger than fiction. Expel a prominent
society member — shortly after I was nominated to be the organization's
president — for being involved with a cancer research organization? Lat-
er, I found myself reflecting on the whole ordeal with a colleague who
knew the inner workings of our society, Professor Sam Tove of North
Carolina State University. He, of course, knew all about the investiga-
tion, as well as other shenanigans. In our discussion, I told him about
AICR being a worthy organization with good intentions. His response
has resonated with me ever since. "It's not about AICR," he said. "It's
about what you did on the National Academy of Sciences report on diet,
nutrition and cancer."

When the NAS's report concluded in June 1982 that a lower intake
of fat and a higher intake of fruits, vegetables and whole grain products
would make for a healthier diet, I had betrayed, in the eyes of some, the
nutrition research community. Supposedly, as one of the two diet and
cancer experimental researchers on the panel, it was my job to protect
the reputation of the American diet as it was. After my failure to do so,
my subsequent involvement with the AICR and its promotion of the
NAS report only made matters worse.

Luckily, reason prevailed in this whole farcical encounter. A board
meeting was held to vote on whether I should be expelled from my so-
ciety, and I handily survived the vote (6-0, with two abstentions).

It was hard not to take all of this personally, but there's a larger point
here, and it's not personal. In the world of nutrition and health, scien-
tists are not free to pursue their research wherever it leads. Coming to
the "wrong" conclusions, even through first-rate science, can damage
your career. Trying to disseminate these "wrong" conclusions to the
public, for the sake of public health, can destroy your career. Mine was
not destroyed — I was lucky, and some good people stood up for me. But
it could have gone much worse.

After all of these numerous ordeals, I have a better understanding of

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why my society did the things it did. The awards funded by Mead John-
son Nutritionals, Lederle Laboratories, BioServe Biotechnologies and
previously Procter and Gamble and the Dannon Institute — all food and
drug outfits — represented a strange marriage between industry and my
society. 8 Do you believe that these "friends" of the society are interested
in pursuing scientific investigation, no matter what the conclusions
may be?

CONSEQUENCES FOR THE PUBLIC

Ultimately, the lessons I learned in my career had little to do with
specific names or specific institutions. These lessons have more to do
with what goes on behind the scenes of any large institution. What
happens behind the scenes during national policy discussions, wheth-
er it happens in scientific societies, the government or in industry
boardrooms, is supremely important for our health as a nation. The
personal experiences 1 have talked about in this chapter — only a sam-
ple of such experiences — have consequences far greater than personal
aggravation and damage to my career. These experiences illustrate the
dark side of science, the side that harms not just individual research-
ers who get in the way, but all of society. It does this by systematically
attempting to conceal, defeat and destroy viewpoints that oppose the
status quo.

There are some people in very influential government and university
positions who operate under the guise of being scientific "experts,"
whose real jobs are to stifle open and honest scientific debate. Perhaps
they receive significant personal compensation for attending to the in-
terests of powerful food and drug companies, or perhaps they merely
have an honest personal bias toward a company-friendly viewpoint.
Personal bias is stronger than you may think. 1 know scientists with
family members who died from cancer and it angers them to entertain
the possibility that personal choices, like diet, could have played a role
in the death of their loved ones. Likewise, there are scientists for whom
the high-fat, high animal-based food diet they eat every day is simply
what they learned was healthy at a young age; they love the habit, and
they don't want to change.

The vast majority of scientists are honorable, intelligent and dedicated
to the search for the common good rather than personal gain. However,
there are a few scientists who are willing to sell their souls to the high-
est bidder. They may not be many in number, but their influence can be

SCIENCE — THE DARK SIDE

267

vast. They can corrupt the good name of institutions of which they are
a part and, most importantly, they can create vast confusion among the
public, which often cannot know who is who. You might turn on the
TV one day to see an expert praising McDonald's hamburgers, and then
read a magazine the same day that you should eat less high-fat red meat
to protect yourself against cancer. Who is to be believed?

Institutions also are part of the dark side of science. Committees like
the Public Nutrition Information Committee and the American Council
on Science and Health generate lopsided panels and committees and
institutions that are far more interested in promoting their point of
view than debating scientific research with an open mind. If a Public
Nutrition Information Committee report says that low-fat diets are
fraudulent scams, and a National Academy of Sciences report says the
opposite, which one is right?

In addition, this closed-mindedness in science spreads across entire
systems. The American Cancer Society was not the only health insti-
tution that worked to make life difficult for the A1CR. The National
Cancer Institute public information office, Harvard Medical School
and a few other universities with medical schools were highly skepti-
cal of the A1CR and, in some cases, outright hostile. The hostility of
medical schools first surprised me, but when the American Cancer
Society, a very traditional medical institution, also joined the fray
it became obvious that there really was a "Medical Establishment."
The behemoth did not take kindly to the idea of a serious connec-
tion between diet and cancer or, for that matter, virtually any other
disease. Big Medicine in America is in the business of treating disease
with drugs and surgery after symptoms appear. This means that you
might have turned on the TV to see that the American Cancer Society
gives almost no credence to the idea that diet is linked to cancer, and
then opened the paper to see that the American Institute for Cancer
Research says what you eat impacts your risk of getting cancer. Who
do you trust?

Only someone familiar with the inside of the system can distinguish
between sincere positions based in science and insincere, self-serving
positions. I was on the inside of the system for many years, working
at the very top levels, and saw enough to be able to say that science
is not always the honest search for truth that so many believe it to be.
It far too often involves money, power, ego and protection of personal
interests above the common good. Very few, if any, illegal acts need to

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occur. It doesn't involve large payoffs being delivered to secret bank
accounts or to private investigators in smoky hotel lobbies. It's not a
Hollywood story; it's just day-to-day government, science and industry
in the United States.

Scientific Reductionism

When our National Academy of Sciences (NAS) Diet, Nutrition and
Cancer Committee was deciding how to summarize the research on diet
and cancer, we included chapters on individual nutrients and nutrient
groups. This was the way research had been done, one nutrient at a
time. For example, the chapter on vitamins included information on
the relationships between cancer and vitamins A, C, E and some B vita-
mins. However, in the report summary, we recommended getting these
nutrients from foods, not pills or supplements. We explicitly stated that
"These recommendations apply only to foods as sources of nutrients —
not to dietary supplements of individual nutrients." 1

The report quickly found its way to the corporate world, which saw
a major money-making opportunity They ignored our cautionary mes-
sage distinguishing foods from pills and began advertising vitamin pills
as products that could prevent cancer, arrogantly citing our report as
justification. This was a great opening to a vast new market — commer-
cial vitamin supplements.

General Nutrition, Inc., the company with thousands of General
Nutrition Centers, started selling a product called "Healthy Greens,"
a multivitamin supplement of vitamins A, C and E, beta-carotene, se-
lenium and a miniscule half-gram of dehydrated vegetables. Then they
advertised their product by making the following claims 2 :

[The Diet, Nutrition and Cancer report] recommended we increase
among other things our amounts of specific vegetables to help
safeguard our bodies against the risk of certain forms of cancer.

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These vegetables recommended by the [National Academy of Sci-
ences report] . . . are the ones we should increase!:] cabbages, Brus-
sels sprouts, cauliflower, broccoli, carrots and spinach Mom

was right!

Research scientists and technicians at General Nutrition Labs,
realizing the importance of the research, instantly went to work
to harness all of the vegetables and combined all of them into a
natural, easy to take potent tablet.

[T]he result is Health Greens [sic], a new potent breakthrough
in nutrition that millions of people can now help safeguard their
well-being with . . . the greens that the [National Academy of Sci-
ences Committee] recommends we eat more of!

GNC was advertising an untested product and improperly using a
government document to support its sensational claims. So the Federal
Trade Commission went to court to bar the company from making these
claims. It was a battle that lasted years, a battle that was rumored to
cost General Nutrition, Inc. about $7 million. The National Academy
of Sciences recommended me as their expert witness because of my co-
authorship of the report in question and because of my harping on this
point during our committee deliberations.

A research associate in my group, Dr. Tom O'Connor, and I spent
three intellectually stimulating years working on this project, including
my three full days on the witness stand. In 1988, General Nutrition,
Inc., settled the false advertising charges relating to Healthy Greens and
other food supplements by agreeing to pay $600,000, divided equally,
to three different health organizations. 3 This was a small price for the
company to pay, considering the ultimate revenues that were generated
by the exploding nutrient supplement market.

FOCUS ON FAT

The focus on individual nutrients instead of whole foods has become
commonplace in the past two decades, and part of the blame can be put
on our 1982 report. As mentioned before, our committee organized the
scientific information on diet and cancer by nutrients, with a separate
chapter for each nutrient or class of nutrients. There were individual
chapters for fat, protein, carbohydrate, vitamins and minerals. I am
convinced it was a great mistake on our part. We did not stress enough
that our recommendations were concerned with whole foods because

SCIENTIFIC REDUCTIONIST

271

many people still regarded the report as cataloging the specific effects of
individual nutrients.

The nutrient that our committee focused on the most was fat. The
first guideline in the report explicitly stated that high fat consumption
is linked to cancer, and recommended reducing our fat intake from 40%
to 30% of calories, although this goal of 30% was an arbitrary cutoff
point. The accompanying text said, "[T]he data could be used to justify
an even greater reduction. However, in the judgment of the committee,
the suggested reduction is a moderate and practical target, and is likely
to be beneficial." One of the committee members, the director of the
United States Department of Agriculture (USDA) Nutrition Laboratory,
told us that if we went below 30%, consumers would be required to re-
duce animal food intake and that would be the death of the report.

At the time of this report, all of the human-based studies showing
fat to be related to cancer (mostly breast and large bowel) were actu-
ally showing that the populations with more cancer consumed not
just more fat, but also more animal-based foods and less plant-based
foods (see chapter four). This meant that these cancers could just as
easily be caused by animal protein, dietary cholesterol, something else
exclusively found in animal-based foods, or a lack of plant-based foods
(discussed in chapters four and eight). But rather than wagging the fin-
ger at animal-based foods in these studies, dietary fat was given as the
main culprit. I argued against putting the emphasis on specific nutrients
in the committee meetings, but only with modest success. (It was this
point of view that landed me the expert witness opportunity at the FTC
hearings.)

This mistake of characterizing whole foods by the health effects of spe-
cific nutrients is what 1 call reductionism. For example, the health effect
of a hamburger cannot be simply attributed to the effect of a few grams
of saturated fat in the meat. Saturated fat is merely one ingredient. Ham-
burgers also include other types of fat, in addition to cholesterol, protein
and very small amounts of vitamins and minerals. Even if you change the
level of saturated fat in the meat, all of the other nutrients are still present
and may still have harmful effects on health. It is a case of the whole (the
hamburger) being greater than the sum of its parts (the saturated fat, the
cholesterol, etc.).

One scientist especially took note 4 of our focused critique of dietary
fat, and decided to test the hypothesis that fat causes breast cancer in
a large group of American women. He was Dr. Walter Willett of the

272

THE CHINA STUDY

Harvard School of Public Health, and the study he used is the famous
Nurses' Health Study.

Starting in 1976, researchers at the Harvard School of Public Health
had enrolled over 120,000 nurses from around the country for a study
that was intended to investigate the relationship between various dis-
eases and oral contraceptives, post-menopausal hormones, cigarettes
and other factors, such as hair dyes. 5 Beginning in 1980, Professor Wil-
lett added a dietary questionnaire to the study and four years later, in
1984, expanded the dietary questionnaire to include more food items.
This expanded dietary questionnaire was mailed to nurses again in 1986
and 1990.

Data now have been collected for over two decades. The Nurses'
Health Study is widely known as the longest-running, premier study
on women's health. 6 It has spawned three satellite studies, all together
costing $4-5 million per year. 6 When I give lectures to health conscious
audiences, upwards of 70% of the people have heard of the Nurses'
Health Study

The scientific community has followed this study closely. The
researchers in charge of the study have produced hundreds of scien-
tific articles in the best peer-reviewed journals. The design of the study
makes it a prospective cohort study, which means it follows a group of
people, a cohort, and records information on diets before disease events
are diagnosed, making the study "prospective." Many regard a prospec-
tive cohort study as the best experimental design for human studies.

The question of whether diets high in fat are linked to breast cancer
was a natural outgrowth of the fierce discussion going on in the mid-
1970s and the early 1980s. High-fat diets not only were associated with
heart disease (the McGovern dietary goals), but also with cancer (the
Diet, Nutrition and Cancer report). What better study to answer this
question than the Nurses' Health Study? It has a good design, massive
numbers of women, top-flight researchers and a long follow-up period.
Sounds perfect, right? Wrong.

The Nurses' Health Study suffers from flaws that seriously doom its
results. It is the premier example of how reductionism in science can
create massive amounts of confusion and misinformation, even when
the scientists involved are honest, well intentioned and positioned at
the top institutions in the world. Hardly any study has done more dam-
age to the nutritional landscape than the Nurses' Health Study, and it
should serve as a warning for the rest of science for what not to do.

SCIENTIFIC REDUCTIONISM

273

CARNIVOROUS NURSES

In order to understand my rather harsh criticism, it is necessary to ob-
tain some perspective on the American diet itself, especially when com-
pared with the international studies that gave impetus to the dietary fat
hypothesis. 7 Americans eat a lot of meat and fat compared to developing
countries. We eat more total protein, and even more significantly, 70%
of our protein comes from animal sources. The fact that 70% of our total
protein comes from animal sources means only one thing: we are con-
suming very few fruits and vegetables. To make matters worse, when
we do eat plant-based foods, we eat a large amount of highly processed
products that often have more added fat, sugar and salt. For example,
the United States Department of Agriculture (USDA) national school
lunch program counts French fried potatoes as a vegetable!

In contrast, people in rural China eat very little animal foods; they
provide only about 10% of their total protein intake. The striking dif-
ference between the two dietary patterns is shown in two ways in Chart
14.1. 8

These distinctions are typical of the dietary differences between
Western cultures and traditional cultures. In general, people in Western
countries are mostly meat eaters, and people in traditional countries are
mostly plant eaters.

So what about the women in the Nurses' Health Study? As you might
guess, virtually all of these women consume a diet very rich in animal-
based foods, even richer than the average American. Their average
protein intake (as % of calories) is around 19%, compared with a U.S.

CHART 14.1: PROTEIN INTAKE IN THE U.S. AND RURAL CHINA 8

100

80
60
40
20
0

ai
+-<
o

China

lAnimal Protein □ Plant Protein

+j
o

CD
Ol
TO

0)
U

CD
Q_

100
80
60
40
20
0

China

I Animal Protein □ Plant Protein

274

THE CHINA STUDY

CHART 14.2: PERCENTAGE OF TOTAL PROTEIN
THAT COMES FROM ANIMAL FOOD

100
90
80
70
60
50
40
30
20
10

O Plant Protein
■ Animal Protein

Nurses

China

average of about 15-16%. To give these figures some perspective, the
recommended daily allowance (RDA) for protein is only about 9-10%.

But even more importantly of the protein consumed by the nurses in this
study, between 78% and 86% comes from animal-based foods, 9 as shown in
Chart 14. 2. 8 ■ 9 Even in the group of nurses that eat the lowest amount of
total protein, 79% of it comes from animal-based foods. 9 In other words,
virtually all of these nurses are more carnivorous than an average American
woman. They consume very few whole, plant-based foods.

This is a crucially important point. To get further perspective, I must
return to the 1975 international comparison by Ken Carroll shown ear-
lier in Charts 4.7 to 4.9. Chart 4.7 is reproduced here in Chart 14.3.

This chart became one of the most influential observations on diet
and chronic disease of the last fifty years. Like other studies, it was a
significant part of the reason why the 1982 Diet, Nutrition and Cancer
report recommended that Americans cut their fat intake to 30% of total
caloric intake in order to prevent cancer. This report and other consen-
sus reports that followed thereafter eventually set the stage for an explo-
sion of low-fat products in the marketplace ("low-fat" dairy products,
lean cuts of meat, "low-fat" sweets and snack foods).

Unfortunately, the emphasis on fat alone was misguided. Carroll's
study, like all the other international comparisons, was comparing
populations that mostly ate meat and dairy to populations that mostly
ate plants. There were many more differences between the diets of these
countries than just the fat intake! What Carroll's graph really shows is

SCIENTIFIC REDUCTIONS

275

a
o
a
o
o
o

o
o

CHART 14.3: FAT INTAKE AND BREAST CANCER MORTALITY

• NETHERLANDS

25 ~| FEMALE «UK • DENMARK

CANADA « • NEW ZEALAND

, nr , ..,^> SWITZERLAND
IRELAND*^ #us

BELGIUM

20 -

AUSTRALIA #^ SWEDEN

AUSTRIA * »• GERMANY
• ITALY NORWAY • FRANCE

1 5 — | »CZECH

• • FINLAND
• PORTUGAL HUNGARY

HONGKONG • POLAND

VENEZUELA •.Va

PANAMA • YUGOSLAVIA ljKttl - t

PHILIPPINES COLOMBIA • PUERTO RICO
* » • • MEXICO
JAPAN • TAIWAN
IU1 ,,... • CEYLON

THAILAND ^EL SALVADOR

1 1 1 1 1 1 1 1 r~

0 20 40 60 80 100 120 140 160 180

Total Dietary Fat Intake (g/day)

that the closer a population gets to consuming a plant-based diet, the
lower its risk of breast cancer.

But because the women in the Nurses' Health Study are so far from a
plant-based diet, there is no way to study the diet and breast cancer rela-
tionship originally suggested by the international studies. There are virtu-
ally no nurses that eat a diet typical of the countries at the bottom of this
graph. Make no mistake about it: virtually this entire cohort of nurses
is consuming a high-risk diet. Most people who look at the Nurses'
Health Study miss this flaw because, as Harvard researchers will point
out, there is a wide range of fat intake among the nurses.

The group of nurses who consume the least fat eat 20-25% of their
calories as fat, and the group of nurses who consume the most fat eat
50-55% of their calories as fat. 10 At a casual glance, this range appears to
indicate substantial differences in their diets, but this is just not true, as
almost all women uniformly eat a diet very rich in animal-based foods.
That begs the question, how can their fat intake vary dramatically while
they all uniformly consume large amounts of animal-based foods?

Ever since "low-fat" became synonymous with "healthy," technology
has created many of the same foods that you know and love, without
the fat. You can now have all kinds of low-fat or no-fat dairy products,
low-fat processed meats, low-fat dressings and sauces, low-fat crackers,
low-fat candies and low-fat "junk food," like chips and cookies. In other

276

THE CHINA STUDY

words, you can eat mostly the same foods as you did twenty-five years
ago, while substantially reducing your fat intake. But you still retain the
same proportion of animal- and plant-based food intakes.

In practical terms this means that beef, pork, lamb and veal consump-
tion is decreasing while lower-fat chicken, turkey and fish consumption
is increasing. In fact, by consuming more poultry and fish, people have
been increasing their total meat intake to record-high amounts, 11 while
trying (and largely failing 12 ) to reduce their fat intake. In addition,
whole milk is being consumed less, but low-fat and skim milk are be-
ing consumed more. Cheese consumption has increased by 150% in the
past thirty years. 13

Overall, we are as carnivorous now as we were thirty years ago, but
we are able to selectively lower our fat intake if we so desire, due to the
wonders of food technology.

To illustrate, we need only to look at two typical American meals. 14, 15
Meal #1 is served in a health-conscious home, where the main grocery
shopper in the family reads the nutrition labels on every food item he or
she buys. The result: a low-fat dining experience.

Meal #2 is served in a home where the standard American fare is ev-
eryone's favorite. When they cook at home, they make the meal "rich."
The result: a high-fat dining experience.

CHART 14.4: LOW-FAT AND HIGH-FAT AMERICAN DINNERS
(ONE PERSON'S DINNER)

Low-Fat Meal #1

High-Fat Meal #2

Dinner

8 oz. roasted turkey

4.5 oz. pan-seared steak

Low-fat gravy

Green beans almondine

Golden roasted potatoes

Herb-seasoned potato
pockets

Beverage

1 cup skim milk

Water

Dessert

Nonfat yogurt

Apple crisp

Reduced-fat cheesecake

Both meals provide roughly 1,000 calories, but are markedly different
in their fat content. The low-fat meal (#1) contains about twenty-five
grams of fat, and the high-fat meal (#2) contains just over sixty grams
of fat. In the low-fat meal, 22% of the total calories come from fat, and
in the high-fat meal, 54% of the calories come from fat.

SCIENTIFIC REDUCTIONISM

277

The health-conscious home has managed to create a meal that is
much lower in fat than the average American dinner, but they've done
it without adjusting their proportionate intakes of animal- and plant-
based foods. Both meals are centered on animal-based foods. In fact,
the low-fat meal actually has more animal-based foods than the high-
fat meal. In effect, this is how the nurses in the Nurses' Health Study
achieved such a wide variation in fat intake. Some nurses simply are
more diligent about choosing low-fat animal products.

Many people would consider the low-fat meal to be a triumph of
healthy meal planning, but what about the other nutrients in these
meals? What about protein and cholesterol? As it turns out, the low-fat
meal contains more than double the protein of the high-fat meal, and almost
all of it comes from animal-based foods. In addition, the low-fat meal con-
tains almost twice as much cholesterol (Chart 14.5). 11 15

CHART 14.5: NUTRIENT CONTENTS OF TWO SAMPLE MEALS

Low-Fat Meal #1

High-Fat Meal #2

Fat [percent of total calories)

22%

54%

Protein
(percent of total calories)

36%

16%

Percentage of total protein
derived from animal-based
foods

93%

86%

Cholesterol

307

165

An overwhelming amount of scientific information suggests that
diets high in animal-based protein can have unfavorable health con-
sequences, as can diets high in cholesterol. In the low-fat meal, the
amount of both of these unhealthy nutrients is significantly higher.

FAT VERSUS ANIMAL FOOD

When women in America, such as those in the Nurses' Health Study
and the billion-dollar 4 Women's Health Trial, 16-19 reduce their fat intake,
they do not do it by reducing their consumption of animal-based foods.
Instead, they use low-fat and nonfat animal products, along with less fat
during cooking and at the table. Thus, they are not adopting the diets
that were shown, in the international correlation studies and in our ru-
ral China study, to be associated with low breast cancer rates.

278

THE CHINA STUDY

This is a very important discrepancy, and is illustrated by the correla-
tion between the consumption of dietary animal protein and dietary fat
for a group of countries (Chart 14. 6). 8 9 ' 18, 20-22 The most reliable com-
parison was published in 1975 20 ; it showed a highly convincing correla-
tion of more than 90%. This means that as fat intake goes up in various
countries, animal protein intake increases in an almost perfectly parallel
manner. Likewise, in the China Study, the intakes of fat and animal pro-
tein also show a similar correlation of 84%. 8 21

In the Nurses' Health Study this is not the case. The correlation
between animal protein and total fat intakes is only about 16%. 9 In
the Women's Health Trial, also including American women, it is even
worse, at -17% 18, 21, 22 ; as fat goes down, animal protein goes up. This
practice is typical of American women who have been led to believe
that, by decreasing their fat intake, they are changing to a healthier diet.
A nurse consuming a "low-fat" diet in the Harvard study like American
women everywhere, is likely to continue eating large amounts of animal
protein, as shown in meal #1 (Chart 14.4).

Sadly, this evidence on the effects of animal-based food on cancer and
other diseases of affluence has been ignored, even maligned, as we con-
tinue to focus on fat and other nutrients in isolation. Because of this, the
Nurses' Health Study and virtually every other human epidemiological
study published to date have been seriously shortchanged in their in-

CHART 14.6: PERCENT CORRELATIONS OF TOTAL FAT
AND ANIMAL PROTEIN CONSUMPTION

100 Y

80-

60-

China

40-

Nurses' Health Study

20-

0-4

International

-20-

Women's Health Study

-40 J

SCIENTIFIC REDUCTIONISM

279

vestigations of diet and disease associations. Virtually all the subjects
under study consume the very diet that causes diseases of affluence. If
one kind of animal-based food is substituted for another, then the ad-
verse health effects of both foods, when compared to plant-based food,
are easily missed. To make matters worse, these studies often focus on
the consumption of just one nutrient, such as fat. Because of these very
serious flaws, these studies have been a virtual disaster for discovering
the really significant effects of diet on these diseases.

THE $100(+) MILLION RESULTS

So now that you know how I interpret the Nurses' Health Study and its
flaws, we should take a look at its conclusions. After more than $100
million and decades of work, there is no shortage of results. So what are
they? The logical place to start is, of course, the question of whether fat
intake really is linked to breast cancer. Here are some of the findings,
cited verbatim:

• "these data provide evidence against both an adverse influence of
fat intake and a protective effect of fiber consumption by middle-
aged women on breast cancer incidence over eight years" 23

Translation: The Nurses' Health Study did not detect a relationship
between dietary fat and fiber and breast cancer risk.

• "we found no evidence that lower intake of total fat or specific major
types of fat was associated with decreased risk of breast cancer" 10

Translation: The Nurses' Health Study did not detect a relationship
between reducingfat, whether it be total fat or certain kinds of fat, and
breast cancer risk.

• "existing data, however, provide little support for the hypothesis
that reduction in dietary fat composition, even to 20% of energy
during adulthood, will lead to a substantial reduction in breast
cancer in Western cultures" 2 ' 1

Translation: The Nurses' Health Study did not detect a breast cancer
association with fat even when women reduced their fat consumption
all the way down to 20% of calories.

280

THE CHINA STUDY

• "relative risks for . . . monounsaturated and polyunsaturated fat . . .
were close to unity" 25

Translation: The Nurses' Health Study did not detect a relationship
between these "good" fats and breast cancer risk.

• "we found no significant associations between intake of meat and
dairy products and risk of breast cancer" 26

Translation: The Nurses' Heath Study did not detect a relationship
between meat and dairy consumption and breast cancer risk.

• "our findings do not support a link between physical activity in
late adolescence or in the recent past, and breast cancer risk among
young adult women" 27

Translation: The Nurses' Health Study did not detect a relationship
between exercise and breast cancer risk.

• "these data are suggestive of only a weak positive association with
substitution of saturated fat for carbohydrate consumption; none
of the other types of fat examined was significantly associated with
breast cancer risk relative to an equivalent reduction in carbohy-
drate consumption" 28

Translation: The Nurses' Health Study detected little or no effect on
breast cancer when women substituted fat for carbohydrates.

• "selenium intake later in life is not likely to be an important factor
in the etiology of breast cancer" 29

Translation: The Nurses' Health Study did not detect a protective effect
of selenium on breast cancer risk.

• "these results suggest that fruit and vegetable consumption during
adulthood is not significantly associated with reduced breast can-
cer risk" 30

Translation: The Nurses' Health Study did not detect a relationship
between fruits and vegetables and breast cancer risk.

So there it is, readers. Breast cancer risk does not rise with increased
intakes of fat, meat, dairy or saturated fat. Breast cancer is not prevented

SCIENTIFIC REDUCTIONISM

281

by increased intakes of fruits and vegetables, or reduced by exercise
(either during the teenage years or during adulthood), dietary fiber,
monounsaturated fats or polyunsaturated fats. Also, the mineral sele-
nium, long considered to be protective of certain cancers, has no effect
on breast cancer. In other words, we might as well conclude that diet is
completely unrelated to breast cancer.

I can understand the frustration of Professor Meir Stampfer, one of
the leading researchers in this group, when he was quoted as saying,
"This has been our greatest failure and disappointment — that we have
not learned more about what people can do to lower their risk." 6 He
was making his comment in response to an opinion that "the single big-
gest challenge for the future [is] sorting out the mess of contradictory
findings and lack of information on breast cancer." 6 1 applaud Professor
Stampfer for his candor, but it's unfortunate that so much money has
been spent to learn so little. Perhaps the most rewarding finding, ironi-
cally, was the demonstration that tinkering with one nutrient at a time,
while maintaining the same overall dietary patterns, does not lead to
better health or to better health information.

Yet Harvard researchers have been steadily cranking out their find-
ings, despite these challenges. From their slew of studies, here are some
findings that I would consider as very troubling contradictions when
comparing disease risks for men versus women:

• Men who consume alcohol three or four times a week have a lower
heart attack risk. 31

• Men with Type 2 diabetes who consume a moderate amount of
alcohol have a lower risk of coronary heart disease. 32

And yet . . .

• Alcohol consumption increases breast cancer incidence by 41%
for women consuming 30-60 g/day of alcohol compared to non-
drinking women. 33

Apparently alcohol is good for heart disease and bad for breast can-
cer. The husband can have a drink with dinner but should never share
it with his wife. Is this a difference between men and women, or is this
a difference in response between heart disease and cancer? Do you feel
more informed or more confused?

Then there are those wonderful omega-3 fatty acids. Some types of
fish contain relatively large amounts of these fats and have been getting

282

THE CHINA STUDY

their share of positive press these days. If you've heard anything about
omega-3 fatty acids, it's that you need more of them to be healthy. Again,
more Harvard findings:

• "... contrary to the predominant hypothesis, we found an in-
creased risk of breast cancer associated with omega-3 fat from fish"
(This increased risk was statistically significant and was associated
with an increase of only 0.1% of the total dietary energy.) 10

• "our findings suggest that eating fish once per month or more can
reduce the risk of ischemic stroke in men" 3 ' 1

• "data suggest that consumption of fish at least once per week may
reduce the risk of sudden cardiac death in men [but not reduce
the] risk of total myocardial infarction, non-sudden cardiac death
or total cardiovascular mortality" 35 (In other words, fish may pre-
vent some aspects of heart disease but ultimately has no effect on
mortality from heart disease, or even heart attack risk.)

Is this yet another question of deciding which disease you fear the
least? Or is this another man versus woman difference?

Here's an even older story: We have been warned for a long time to
cut down on our cholesterol intake, and it was largely for this reason
that consumption of eggs was brought into question. One egg has a
whopping 200 mg or more of cholesterol, 36 which takes up a large pro-
portion of our 300 mg recommended daily limit. So, what do the Har-
vard studies tell us on this timeworn issue?

. . . consumption of up to one egg per day is unlikely to have sub-
stantial overall impact on the risk of CHD or stroke among healthy
men and women 37

But, for breast cancer,

Our findings [representing eight prospective studies] suggest a possi-
ble modest increase in [breast cancer] risk with egg consumption

breast cancer risk was found to increase by 22% with every 100-g
per day increment of egg consumption [about 2 eggs] 26 [There was
a 67% increase in risk for the Nurses' Health Study. ] 26

But earlier, the Harvard researchers took a slightly different position:

...among healthy men and women, moderate egg consumption
can be part of a nutritious and balanced diet 38

SCIENTIFIC REDUCTIONISM

283

Most recently, the Nurses' Health Study is cited as having come up
with an even more powerful endorsement for eggs. A recent news item
stated:

Eating eggs during adolescence could protect women against
breast cancer 39

The article goes on to quote a Harvard researcher as saying:

Women who had, during adolescence, a higher consumption of
eggs . . . had a lower risk of breast cancer 39

Most people who read this news article will likely say that eggs are
back in favor — even when they don't know how many eggs per day are
okay or whether there are exceptions to this generalization. Eggs will
only seem to be more healthful when the henhouse industry adds their
words of wisdom. But wait a minute — evidence says egg consumption
for teenage girls is okay, maybe even good, but evidence also says more
egg consumption overall increases breast cancer risk. By the way, here's
something else to think about. Multiple studies have rather consistently
shown that egg consumption can increase colon cancer risk, more so for
women than for men. 40

What are we to believe? One minute alcohol intake can reduce our
disease risks, the next minute it can increase them. One minute fish
consumption can help to reduce our disease risks, the next minute it
can hurt. One minute eggs are bad, the next minute they can be healthy.
It seems to me that what is missing here is the larger context. What you
have without that context is just a lot of confusion.

UNRAVELING DIET AND CANCER

In addition to stating that diet and exercise are unrelated to breast can-
cer, the Harvard researchers have been chipping away at other popular
notions regarding diet and cancer. For example, the Harvard studies
have not been able to detect any association between colorectal cancer
and fiber or fruit and vegetable intake. 4, 41,42

Dietary fiber, of course, only comes from plant-based foods, thus
these findings put a dent in the idea that fiber or fruits, vegetables and
cereals prevent large bowel cancer. Keep in mind that the Harvard stud-
ies are dealing with uniformly carnivorous populations, almost none
of which are using a whole foods, plant-based diet that is naturally low
in fat and high in fiber. It is likely that the potential protective effect of

284

THE CHINA STUDY

fiber or fruits and vegetables does not kick in against colorectal cancer
until there is a complete dietary shift away from an animal-based diet.

Between the colon cancer and breast cancer findings, the Nurses'
Health Study has done much to confuse, if not discredit, the idea that
diet is related to cancer. After these decades of work, Professor Walt
Willett says:

. . . increasing fruits and vegetables overall appears to be less prom-
ising as a way to substantially reduce cancer risk the benefits

[of these foods] appear greater for cardiovascular disease than for
cancer 4

This statement sounds a bit ominous. Colon cancer, historically one
of the first cancers said to be prevented by a plant-based diet, 43-45 now is
being said to be unrelated to diet? And low-fat diets don't prevent breast
cancer? With results like these, it's only a matter of time before the hy-
pothesis of a dietary connection to cancer starts falling apart. In fact, I
have already heard people within the scientific community beginning to
say that diet may have no effect on cancer.

These are the reasons that I believe that the Nurses' Health Study has
done considerable damage to the nutrition landscape. It has virtually
nullified many of the advances that have been made over the past fifty
years without actually posing a scientifically reliable challenge to earlier
findings regarding diet and cancer.

This problem of studying a population that uniformly consumes a
high-risk diet and looking at the differences in consumption of one nu-
trient at a time is not unique to the Nurses' Health Study. It is common
to virtually all studies using Western subjects. Furthermore, there is
little or no value to pooling the results of many large studies for analysis
in order to get a more reliable result if all the studies have the same flaw.
A pooling strategy is often used for identifying cause-and-effect associa-
tions that are more subtle and uncertain within single studies. This is a
reliable assumption when each study is properly done, but obviously it
is not when all the studies are similarly flawed. The combined results
only give a more reliable picture of the flaw.

The Harvard researchers have done several of these multi-study
pooled analyses. One such pooled analysis concerned the question of
whether meat and dairy foods had any effect on breast cancer. 26 A previ-
ous 1993 pooling of nineteen studies 46 had shown a modest, statistically
significant 18% increase in breast cancer risk with increased meat intake

SCIENTIFIC REDU CTION ISM

285

and 17% increase with increased milk intake. 46 The Harvard researchers
therefore summarized in 2002 a more recent group of studies, this time
including eight large prospective studies where dietary information was
thought to be more reliable and where a much larger group of women
was included. The researchers concluded:

We found no significant association between intake of meat or
dairy products and risk of breast cancer. 26

Most people would say, "Well, that's it. There is no convincing evi-
dence that meat and dairy foods are associated with breast cancer risk."
But let's take another look at this supposedly more sophisticated analy-
sis.

All eight of these studies represented diets that had a high proportion
of animal-based foods. In effect, each study in this pool was subject to
the same flaw from which the Nurses' Health Study suffered. It makes
no sense, and does no good, to combine them. In spite of there being
351,041 women and 7,379 breast cancer cases in this mega-database,
these results cannot detect the true effect of diets rich in meat and dairy
on breast cancer risk. This would be true even if there were a few mil-
lion subjects in the study. Like the Nurses' Health Study, these studies
all involved typical Western diets highly skewed toward the consump-
tion of animal-based foods, where people are tinkering with the intake
of only one nutrient or one food at a time. Every study failed to take
into account a broader range of dietary choices — including those which
demonstrated positive effects on breast cancer risk in the past.

IGNORING MY CRITIQUE

Once, after reading a publication on animal protein and heart disease
in the Nurses' Health Study 9 1 published a critique 47 summarizing some
of the same points that I am making in this chapter, including the in-
ability of the Nurses' Health Study to advance our understanding of
the original international correlation studies. They responded, and our
exchange is as follows.
First, my comment:

Within a dietary range [so rich in animal-based foods] , it makes no
sense to me that it is possible to reliably detect the so-called inde-
pendent associations of the individual constituents of this group
when it can be expected that they share the same disease outcomes

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and when there are so many difficult-to-measure and interacting
risk factor exposures. When will it be understood that it is the to-
tal diet and the aggregate and comprehensive effects of large food
groups that make the greatest contribution to the maintenance
of health and prevention of disease? The sort of reductionism
embodied in the interpretation of data from this [Nurses' Health
Study] cohort runs the risk of severely misleading discourse on
meaningful public health and public policy programs. 47

Then the response from Dr. Hu and Professor Willett:

Although we agree that overall dietary patterns are also important
in determining disease risk (ref. cited), we believe that identifica-
tion of associations with individual nutrients should be the first
step because it is the specific compounds or groups of compounds
that are fundamentally related to the [disease process]. Specific
components of diet can be modified, and individuals and the food
industry are actively doing so. Understanding the health effects of
specific dietary changes, which Campbell refers to as "reduction-
ism," is therefore an important undertaking. 48

I agree that studying the independent effects of individual food
substances (their identities, functions, mechanisms) is worthwhile,
but Willett and I sharply disagree with how to interpret and use these
findings.

I strongly reject the implications in Willett's argument that "specific
components of the diet can be modified" to the benefit of one's health.
This is precisely what is wrong with this area of research. In fact, if the
Nurses' Health Study shows nothing else, it demonstrates that modify-
ing the intake of one nutrient at a time, without questioning whole di-
etary patterns, does not confer significant health benefits. Women who
tinker with fat, while maintaining a near-carnivorous diet, do not have
a lower breast cancer risk.

This gets to the heart of reductionism in science. As long as scientists
study highly isolated chemicals and food components, and take the infor-
mation out of context to make sweeping assumptions about complex diet
and disease relationships, confusion will result. Misleading news head-
lines about this or that food chemical and this or that disease will be the
norm. The more impressive message about the benefits of broad dietary
change will be muted as long as we focus on relatively trivial details.

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287

On occasions, when our paths have crossed, Professor Willett and
I have had discussions about the findings on fat as they relate to the
China Study and the Nurses' Health Study. I have always made the same
point: whole foods, plant-based diets, naturally low in fat, are not in-
cluded in the Nurses' Health Study cohort, and that it is these types of
diets that are the most beneficial for our health. Professor Willett has
said to me, in response, on more than one occasion, "You may be right,
Colin, but people don't want to go there." This comment has disturbing
implications.

Scientists should not be ignoring ideas just because we perceive that
the public does not want to hear them. Too often during my career, ]
have heard comments that seem to be more of an attempt to please the
public than to engage in an open, honest debate, wherever it may take
us. This is wrong. The role of science in a society is to observe, to ask
questions, to form and test hypotheses and to interpret the findings
without bias — not to kowtow to people's perceived desires. Consumers
have the ultimate choice of whether to integrate our findings into their
lifestyles, but we owe it to them to give them the best information pos-
sible with which to make that decision and not decide for them. It is
they who paid for this research and it is only they who have the right to
decide what to do with it.

The perception in the scientific community that the public only
wants magic bullets and simple dietary tinkering is overrated. I have
learned in my public lectures that there is more interest in diet/lifestyle
change than the academic community is willing to admit.

This method of investigating details out of context, what I call reduction-
ism, and trying to judge complex relationships from the results is deadly.
It is even more damaging than the misbehavior of the small minority
of scientists I discussed in chapter thirteen. Unfortunately, this flawed
way of investigating nutrition has become the norm. As a consequence,
honest, hardworking, well-intentioned scientists around the world are
forced to make judgments about whole dietary effects on the basis of
narrowly focused studies on individual nutrients. The greatest danger is
that reductionism science, standing naked from its larger environment,
has come to be the gold standard. Indeed, I know many researchers who
would even say that this is what defines "good" science.

These problems are especially egregious in the investigation of vi-
tamin supplements. As I noted at the beginning of the chapter, I spent
over three years during the early history of the nutrient supplement

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business developing testimony for the Federal Trade Commission and
the National Academy of Sciences in their court case against General
Nutrition, Inc. I argued that specific health benefits for chronic diseases
could not be claimed for isolated vitamins and minerals in supplement
form. For this, I took a lot of heat from my colleagues who believed
otherwise. Now, more than fifteen years later, after hundreds of millions
of dollars of research funding and billions of dollars of consumer spend-
ing, we now have this conclusion from a recent survey of the evidence:

The U.S. Preventive Services Task Force (USPSTF) concludes that
the evidence is insufficient to recommend for or against the use of
supplements of A, C or E; multivitamins with folic acid; or antioxi-
dant combinations for the prevention of cancer or cardiovascular
disease. 49 - 50

How many more billions of dollars must be spent before we under-
stand the limitations of reductionist research? Scientific investigations
of the effects of single nutrients on complex diseases have little or no
meaning when the main dietary effect is due to the consumption of
an extraordinary collection of nutrients and other substances found in
whole foods. This is especially true when no subjects in the study popu-
lation consume a whole foods, plant-based diet when it is this diet that
is most consistent with the biologically-based evidence, supported by
the most impressive array of professional literature, consonant with the
extremely low disease rates seen in the international studies, far more
harmonious with a sustainable environment, possessed of the power to
heal advanced disease, and has the potential, without parallel, for sup-
porting a new, low-cost health care system. I categorically reject the idea
of doing reductionism research in this field without seeking or under-
standing the larger context. The endless stream of confusion generated
by misinterpreted reductionism undermines not only the entire science
of nutrition, but also the health of America.

The "Science" of Industry

What does every American spend money on several times a day? Eating.
After a lifetime of eating, what do we all do? Die — a process that usu-
ally involves large costs as we try to postpone it for as long as possible.
We're all customers of hunger and death, so there's a lot of money to be
spent and made.

Because of this, the food and health industries in America are among
the most influential organizations in the world. The revenue generated
by the companies that produce food and health products is stagger-
ing. Many individual food companies have over $10 billion in annual
revenues. Kraft has revenues of roughly $30 billion a year. The Danone
Group, an international dairy company based in France, operates the
Dannon brand and has revenues of $15 billion a year. And of course,
there are the large fast food companies. McDonald's has revenues in ex-
cess of $ 15 billion a year, and Wendy's International generates almost $3
billion a year. Total food expenditures, including food bought by individu-
als, government and business, exceed $700 billion a year. 1

The massive drug company Pfizer had $32 billion in revenue in 2002,
while Eli Lilly & Co. chalked up over $11 billion. Johnson and Johnson
collected over $36 billion from selling their products. It's not an over-
statement to say over a trillion dollars every year is riding on what we
choose to eat and how we choose to treat sickness and promote health.
That's a lot of money.

There are powerful players that compete for your food and health

289

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THE CHINA STUDY

dollars. Individual companies, of course, do what they can to sell more
of their products, but also there are industry groups that work to in-
crease general demand for their products. The National Dairy Council,
National Dairy Promotion and Research Board, National Fluid Milk
Processor Promotion Board, International Sprout Growers Associa-
tion, American Meat Institute, Florida Citrus Processors Association,
and United Egg Producers are examples of such industry groups. These
organizations, operating independently of any single company, wield
significant influence — the most powerful among them have yearly bud-
gets in the hundreds of millions of dollars.

These food companies and associations use whatever methods they
can to enhance their products' appeal and grow their market. One way
to accomplish this is to claim nutritional benefits for the food products
they sell. At the same time, these companies and associations must
protect their products from being considered unhealthy. If a product is
linked to cancer or some other disease, profits and revenue will evapo-
rate. So food business interests need to claim that their product is good
for you, or, at least, that it's not bad for you. In this process, the "sci-
ence" of nutrition becomes the "business" of marketing.

THE AIRPORT CLUB

While I was getting the China Study off the ground, I learned of a com-
mittee of seven prominent research scientists who had been retained
by the animal-based foods industry (the National Dairy Council and
the American Meat Institute) to keep tabs on any research projects in
the U.S. likely to cause harm to their industry. I knew six of the seven
members, four of them quite well. A graduate student of mine was visit-
ing with one of these scientists and was given a file on the committee
activity. I have never learned exactly why the file passed hands. Perhaps
the scientist's conscience was getting the better of him. In any case, the
file was ultimately given to me.

The file contained minutes of committee meetings, the latest being
held at Chicago's O'Hare Airport. From then on, I have called this group
of scientists "The Airport Club." It was run by Professors E. M. Foster
and Michael Pariza, faculty members of the University of Wisconsin
(where Alf Harper was located), and was funded by the meat and dairy
industry. This committee's main objective was to have members observe
projects that might do "harm" to their industry. With such surveillance,
the industry could more effectively respond to unexpected discoveries

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291

from researchers that might make otherwise unanticipated news. 1 had
learned well that, when the stakes are high, industry was not averse to
putting its own spin on a story.

They listed about nine potentially damaging projects, and I had the
dubious distinction of being the only researcher responsible for two
of the projects. I was named once for the China Study, which one of
the members was assigned to watch over, and once for my association
with the American Institute for Cancer Research (AICR), especially my
chairing of the review panel that decided which research applications
on diet and cancer got funded. Another panel member had the task of
keeping an eye on the AICR activity.

After learning of The Airport Club, and of the individual assigned to
watch over me at the AICR grant meetings, I was in a position to see
how his spying was going to unfold. I went into the first AICR review
panel meeting after learning of the Club with an eye on the spy who was
keeping an eye on me!

One might argue that this industry-funded "spying" was not illegal,
and that it is prudent for a business to keep tabs on potentially damag-
ing information that might affect its future. I agree completely, even if
it was disconcerting to find myself on the list of those being spied on.
But industry does more than just keep tabs on "dangerous" research. It
actively markets its version, regardless of potentially disastrous health
effects, and corrupts the integrity of the science to do so. This is espe-
cially troubling when academic scientists do the spying and hide their
intentions.

POWERFUL GROUPS

The dairy industry, one of the sponsors of The Airport Club, is particu-
larly powerful in this country. Founded in 1915, the well-organized,
well-funded National Dairy Council has been promoting milk for al-
most a hundred years. 2 In 1995, two major milk industry groups put
a new face on their old establishment, renaming it Dairy Management,
Inc. The purpose of this new group was "to do one thing: increase de-
mand for U.S.-produced dairy products," to cite their Web site. 3 They
had a 2003 marketing budget of more than $165 million to do it. 4 In
comparison, the National Watermelon Promotion Board has a budget
of $1.6 million. 5 A Dairy Management, Inc., press release includes the
following items 4 :

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Rosemont, Illinois — National, state and regional dairy producer
directors have approved a budget of $165.7 million for a 2003
Unified Marketing Plan (UMP) designed to help increase dairy

demand

. . . Major program areas include:

Fluid Milk: In addition to key ongoing activities in advertising,
promotion and public relations efforts targeted to children ages six
to twelve and their mothers, 2003 dairy checkoff efforts will focus
on developing and extending partnerships with major food mar-
keters, including Kellogg's®, Kraft foods® and McDonald's®

. . . School Marketing: As part of an effort to guide school-age
children to become life-long consumers of dairy products, 2003
activities will target students, parents, educators and school food-
service professionals. Programs are underway in both the class-
room and the lunchroom, where dairy checkoff organizations look
to widen the success of last year's School Milk Pilot Test

. . . Dairy Image/Confidence: This ongoing program area aims
to protect and enhance consumer confidence in dairy products
and the dairy industry. A major component involves conducting
and communicating the results of dairy nutrition research show-
ing the healthfulness of dairy products, as well as issues and crisis
management

If I may paraphrase the dairy industry's efforts: their goals are to 1)
market to young children and their mothers; 2) use schools as a chan-
nel to young customers; 3) conduct and publicize research favorable to
the industry.

Many people are not aware of the dairy industry's presence in our
schools. But make no mistake: on nutrition information, the dairy in-
dustry reaches young children more effectively than any other indus-
try.

The dairy industry has enlisted the public education system as the
primary vehicle for increasing demand for its products. The 2001 Dairy
Management, Inc., annual report stated 6 :

As the best avenue to increase fluid milk consumption long-term,
children are without a doubt the future of dairy consumption.
That's why the dairy checkoff continues to implement school milk
marketing programs as one way to help increase kids' fluid milk
consumption.

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293

Dairy producers . . . launched two groundbreaking initiatives in
2001. A yearlong school milk research program that began in the
fall of 2001 examines how improved packaging, additional flavors,
coolers with merchandising and better temperature regulation can
affect fluid milk consumption and kids' attitudes toward milk both
in and out of school. The study concludes at the end of the 2001-
02 school year. Also, dairy producers and processors worked to-
gether to conduct a five-month vending study in middle and high
schools in five major U.S. markets. The study revealed that many
students would choose milk over competitive beverages if it were
available when, where and how they wanted.

Many other successful school programs continue to encourage chil-
dren to drink milk. Nutrition education programs, such as "Pyramid
Explorations" and "Pyramid Cafe," teach students that dairy products
are a key part of a healthy diet; the "Cold Is Cool" program teaches
school cafeteria managers how to keep milk cold, just how kids like
it; and the checkoff is helping expand dairy-friendly school breakfast
programs. In addition, the popular "got milk" campaign continues to
reach children at school and through such kid-focused media outlets as
Nickelodeon and the Cartoon Network.

These activities are far from small-scale; in 1999, "Chef Combo's
Fantastic Adventures," an "educational" (marketing) set of lesson
plans produced by the dairy industry, "was placed in 76% of preschool
kindergarten sites nationally." 7 According to a dairy industry report to
Congress, 8 the dairy industry's "nutrition education" programs are do-
ing quite well:

"Pyramid Cafe®" and "Pyramid Explorations™," targeted to sec-
ond and fourth grades, reach over 12 million students with mes-
sages that milk and dairy products are a key part of a healthy diet.
Survey results continue to show a very high utilization rate for
these two programs, currently at over 70% of the instructors that
have the programs.

America is entrusting the important task of educating our children
about nutrition and health to the dairy industry. In addition to ubiquitous
nutrition lesson plans and "educational" kits, the industry supplies high
schools with videos, posters and teaching guides regarding nutrition; it
runs special promotions in cafeterias to increase milk consumption in

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thousands of schools; it distributes information to principals at national
conferences; it runs back-to-school promotions with over 20,000 schools;
and it runs sports promotions targeted toward youth.

Should we be worried? In a word, yes. If you are curious as to what
kind of "education" is being taught by the dairy industry, take a look at
their Web site. 9 When I visited the site in July 2003, one of the first bits
of information to greet me was, "July is National Ice Cream Month."
Upon clicking for more information on National Ice Cream Month, I
read, "If you're wondering if you can have your ice cream and good
nutrition too, the answer is 'yes'!" 9 Great. So much for combating child-
hood obesity and diabetes!

The Web site is divided up into three sections, one for educators, one
for parents and one for food service professionals. When I looked at the
Web site in July 2003 (the Web site regularly changes its content), in
the educator portion of the site, teachers could download lesson plans
to teach nutrition to their classrooms. Lesson plans included making
hand puppets of cows and dairy foods and doing a finger play Once
the puppets are made, the teacher should "[t]ell the students they're
going to meet five special friends, and these friends want boys and girls
to grow up to be strong and healthy." 9 Another lesson was "Dairy Treat
Day," where each child gets to taste cheese, pudding, yogurt, cottage
cheese and ice cream. 9 Or teachers could lead their classes in making
"Moo Masks." 9 For the more advanced fourth grader, teachers could do
a lesson plan from Pyramid Explorations in which students explore the
five food groups, and their health benefits, as follows 9 :

Milk Group (Build strong bones and teeth.)
Meat Group (Build strong muscles.)
Vegetable Group (Help you see in the dark.)
Fruit Group (Help heal cuts and bruises.)
Grain Group (Give us energy.)

Based on the evidence presented in the previous chapters, you know
that if this is what our children are learning about nutrition and health
then we are in for a painful journey, courtesy of Dairy Management,
Inc. Obviously neither kids nor their parents are learning about how
milk has been linked to Type 1 diabetes, prostate cancer, osteoporosis,
multiple sclerosis or other autoimmune diseases, and how casein, the
main protein in dairy foods, has been shown to experimentally promote
cancer and increase blood cholesterol and atherosclerotic plaque.

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295

In 2002, this marketing Web site delivered over 70,000 lesson plans to
educators. 8 The dairy industry truly is teaching its version of nutrition
to the next generation of Americans.

The industry has been doing this for decades, and it has been suc-
cessful. I have encountered many people who, when they hear about the
potential adverse effects of dairy foods, immediately say, "Milk can't be
bad." Usually these people don't have any evidence to support their po-
sition; they just have a feeling that milk is good. They've always known
it to be that way, and they like it that way. You can trace some of their
opinions back to their school days, when they learned that there are
seven continents, two plus two equals four, and milk is healthy. If you
think about it this way, you will understand why the dairy industry has
had such exceptional influence in this country by using education for
its marketing purposes.

If this marketing program weren't such a widespread threat to our
children's health, it would be downright laughable that an industry
group would try to peddle its food product under such a thinly-veiled
"education" plan. Don't people wonder what's going on when almost ev-
ery single children's book advertised in the "Nutrition Bookshelf por-
tion of this Web site revolved around either milk, cheese or ice cream,
with such titles as Ice Cream: Great Moments in Ice Cream History? 9 After
all, during July 2003 there were no vegetable books anywhere to be
found on this "Nutrition Bookshelf! Aren't they healthy?

At least when the dairy industry describes all of these school-related
activities in the official reports to Congress and in industry press re-
leases, it rightly refers to them as "marketing" activities.

CONJUGATED LINOLEIC ACID

The dairy industry doesn't stop with kids. For adults, the industry puts
a heavy emphasis on "science" and the communication of research re-
sults that might be construed as showing health benefits from eating
dairy foods. The dairy industry spends $4 to $5 million a year to fund
research towards the goal of finding something healthy to talk about. 7
10 In addition, the dairy industry promoters employ a Medical Advisory
Board made up of doctors, academics and other health professionals.
These scientists are the ones who appear as medical professionals in
the media, providing science-based statements supporting the health
benefits of milk.

The Airport Club was a good example of industry efforts to maintain

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favorable product image and "confidence." In addition to keeping an
eye on potentially damaging projects, the Club was trying to generate
research that might show that cancer could be prevented by drinking
cow's milk. What a coup that would be! At that time, the industry was
getting quite edgy about the growing evidence showing that the con-
sumption of animal-based foods is associated with cancer and related
ailments.

Their hook for this research was an unusual group of fatty acids
produced by bacteria in the cow's rumen (the biggest of the four stom-
achs). These fatty acids were collectively called conjugated linoleic acid
(CLA), which is produced from the linoleic acid commonly found in
corn that the cow eats. From the cow's rumen, CLA is then absorbed
and gets stored in the meat and milk of the animal, eventually to be
consumed by humans.

The big payday for The Airport Club was when initial tests on ex-
perimental mice suggested that CLA might help to block the formation
of stomach tumors produced by a weak chemical carcinogen called
benzo(a)pyrene. u ' 12 But there was a catch in this research. The catch
was that researchers gave CLA to the mice first, and then gave the car-
cinogen benzo(a)pyrene. The ordering of these chemical feedings was
backwards. In the body there is an enzyme system that works to minimize
the amount of cancer caused by a carcinogen. When a chemical such as
CLA is initially consumed, it "excites" that enzyme system so that it has
increased activity. So the trick was to administer CLA first, to excite the
enzyme system, and then administer the carcinogen. In this order, the en-
zyme system excited by CLA would be more effective at getting rid of the
carcinogen. As a result, CLA could be called an anticarcinogen.

Let me give you an analogous situation. Let's say you have a bag of a
potent pesticide in your garage. The pesticide bag says, "Do not swal-
low! In case of ingestion, contact your local poison control health au-
thorities," or some such warning. But let's say you're hungry and you eat
a handful of pesticide anyway. That pesticide in your body will "rev up"
the enzyme systems in all of your cells that are responsible for elimi-
nating nasty things. If you then go inside and eat a handful of peanuts
dripping with aflatoxin, your body's enzyme systems will be primed to
deal with the aflatoxin, and you'll end up with fewer aflatoxin-induced
tumors. So, the pesticide, which will ultimately do all sorts of nasty
things in your body, is an anticarcinogen! This scenario is obviously
absurd, and the research on mice that initially showed CLA to be an

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297

anticarcinogen was similarly absurd. However, the end results of the
mice research sounded pretty good to people who don't know this
methodology (including most scientists).

Airport Club member Michael Pariza headed the research that stud-
ied CLA in some detail. 13-15 Later, at Roswell Park Memorial Institute
for Cancer Research in Buffalo, a very good researcher and his group
extended the research still further and demonstrated that it did more
than merely block the first step in the formation of tumors. CLA also
appeared to slow down subsequent tumor growth 16 ' 17 when fed after
the carcinogen. This was a more convincing finding of the anticancer
properties of CLA than the initial studies, 11 ' 12 which showed only an
inhibition of tumor initiation.

Regardless of how promising these mouse and cow studies were be-
coming, this research remained two major steps removed from human
cancer. First, it had not been shown that cow's milk containing CLA,
as a whole food (as opposed to the isolated chemical CLA), prevents
cancer in mice. Second, even if such an effect existed in mice, it would
need to be confirmed in humans. In fact, as has been discussed earlier
in this book, if cow's milk has any effect at all, it has been shown to in-
crease, not decrease, cancer. The far more significant nutrient in milk is
protein, whose potent cancer-promoting properties are consistent with
the human data.

In other words, to make any health claims regarding CLA in milk
and its effect on human cancer would require unreasonably large leaps
of faith. But never doubt the tenacity (i.e., money) of those who would
like to have the public believe that cow's milk prevents cancer. Lo and
behold, a recent front-page headline in our local newspaper, the Ithaca
Journal, stated "Changing Cows' Diets Elevates Milk's Cancer-Fight-
ing." 18 This article concerned the studies of a Cornell professor who was
instrumental in the development of bovine growth hormone now fed to
cows. He showed that he could increase CLA in cow's milk by feeding
the animals more corn oil.

The Ithaca Journal article, although only in a local, hometown news-
paper, really was a dream come true for the sponsors of The Airport
Club. The headline delivers a powerful but very simple message to the
public: drinking milk reduces cancer risk. I know that media people
like punchy statements so, initially, I suspected that the reporter had
made claims beyond what the researchers had said. But in the article the
enthusiasm expressed by Professor Bauman for the implications for this

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research equaled that of the headline. The study cited in this article only
showed that CLA is higher in the milk of cows fed corn oil. That's a long
way from having any relevance to human cancer. No studies had yet
shown that humans or even mice drinking cow's milk had a lower risk
of cancer — of any kind. Yet Bauman, who is a technically competent
researcher, was quoted as saying that these findings have "good poten-
tial because CLA happens to be [a] very potent [anticarcinogen]." The
journalist went on to say "CLA has been shown to suppress carcinogens
and inhibit the spread of colon, prostate, ovarian and breast cancers and
leukemia," and concluded that "all indications are that CLA is effec-
tive in humans even in low concentrations." According to the article,
Bauman says that this "research represents the new focus on designing
foods to enhance their nutritional and health qualities." These claims
could not be more dramatic, considering the absence of the necessary
human research.

Bauman, Pariza and their many other colleagues 19 have vigorously
pursued this line of research for fifteen years and have published a large
number of research papers. Although additional beneficial effects of
CLA are said to exist, the key research still has not been done, namely,
testing whether the consumption of milk from cows fed high-corn oil
diets really will reduce human cancer risk.

More recently, Bauman and his colleagues have attempted to take a
step toward finding this essential connection. They have shown that
the milk fat of cows fed high amounts of corn oil (i.e., linoleic acid, the
parent of CLA), like synthetic CLA, was able to decrease tumors in rats
treated with a carcinogen. 20 But again, they used the tricky experimental
method. They administered the milk fat before, not after the carcinogen.
Yet their claims will be as dramatic as ever, because this is the first time
that CLA, as present in food (i.e., the fat), is shown to be as anticarcino-
genic as the isolated chemical. Translated: eat butter from cows fed corn
oil — it prevents cancer!

THE SCIENCE OF INDUSTRY

The CLA story is a good example of how industry uses science to in-
crease demand for its product in order to make more money. At the very
least, industry science often leads to public confusion (Are eggs good?
Are they bad?), and at its worst, industry science leads unsuspecting
consumers to foods that are actually bad for them, all in the name of
better health.

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299

Conflicts of interest abound in this science of industry. The CLA re-
search was created with special interest money and has grown and been
sustained with special interest money. The National Dairy Council, 20-22
Kraft Foods, Inc., 20 the Northeast Dairy Foods Research Center, 20 ' 21
the Cattlemen's Beef Board 23 and the Cattlemen's Beef Association 23 are
groups that have frequently funded these studies.

Corporate influence in the academic research world can take many
forms, ranging from flagrant abuses of personal power to conflicts of
interest, all hidden from public view. This influence does not need to be
a crass payoff to researchers to fabricate data. That sort of behavior is
rare. The more significant way for corporate interests to influence aca-
demic research is much more sophisticated and effective. As illustrated
by the CLA example, scientists investigate a detail out of context that
can be construed as a favorable message and industry exploits it for all
it's worth. Almost no one knows where the CLA hypothesis started and
who originally funded it.

Few people really question such research if it is published in the best
journals. Very few people, especially among the public, know which
studies are "benefiting" from direct corporate funding. Very few people
are able to sort out the technical details and recognize the missing in-
formation that would otherwise establish context. Almost everyone,
however, understands that headline in my local newspaper.

I could play this game, too. If I wanted to hurt the dairy industry and
be a little wild in my interpretation of study results, I could produce an-
other headline to say, "New birth control chemical discovered in cow's
milk." Recent research, for example, showed that CLA dramatically kills
chick embryos. 13 Also, CLA increases the tissue level of saturated fats
that could (using our dramatic method of interpretation) exacerbate
heart disease risk. Of course, I have taken these two unrelated effects
grossly out of context in my example. I don't really know whether these
CLA effects actually translate into less fertility and more heart disease
for humans, but if I were playing the game the way industry enthusiasts
do, I wouldn't mind. It would make a great headline, and that can go a
long way.

I recently met with one of the members of The Airport Club, a scien-
tist who has been involved in the CLA effort, and he confessed that the
CLA effect will never be anything more than a drug effect. However, you
can bet that what is known in private will not be told in public.

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INDUSTRY'S LOVE OF TINKERING

Much of The Airport Club and the CLA story is a story about the "dark
side" of science, which I detailed in chapter thirteen. But the CLA story
is also about the dangers of reductionism, of taking details out of con-
text and making claims about diet and health, which I discussed in the
previous chapter. Like academia, industry is also an essential player in
the system of scientific reductionism that undermines the knowledge
we have about dietary patterns and disease. Industry, you see, loves to
tinker. Securing patents based on details leads to marketing claims and,
ultimately, to greater revenues.

In a recent paper 20 by several CLA researchers (including Professor
Dale Bauman, a long-time friend of the animal foods industry), the fol-
lowing sentence appeared, revealing much about how some industry
enthusiasts feel as we "tinker" our way to health:

The concept of CLA-enriched foods could be particularly appeal-
ing to people who desire a diet-based approach to cancer preven-
tion without making radical changes in their eating habits. 20

I know that, for Bauman and others, "making radical changes
in . . . eating habits" means consuming a diet rich in plant-based foods.
Rather than avoiding bad foods altogether, these researchers are sug-
gesting that we tinker with the existing, but problematic, foods to cor-
rect the problem. Instead of working with nature to maintain health,
they want us to rely on technology — their technology.

This faith in technological tinkering, in man over nature, is ever-
present. It is not limited to the dairy industry, or the meat industry, or
the processed foods industry. It has become part of every single food
and health industry in the country, from oranges to tomatoes, from cere-
als to vitamin supplements.

The plant food industry got carried away recently when another ca-
rotenoid was "discovered." You've probably heard of it. It is called lyco-
pene, and it provides the red color in tomatoes. In 1995, it was reported
that people who ate more tomatoes, including whole tomatoes and
tomato-containing foods like pasta sauces, had a lower risk for prostate
cancer, 24 supporting an earlier report. 25

For those companies that make foods with tomato products, this was
a gift from above. Marketing people in the corporate world quickly got
the message. But what they zeroed in on was lycopene, not tomatoes.

THE "SCIENCE" OF INDUSTRY

301

The media, willing to oblige, rose to the occasion. It was lycopene time!
Suddenly lycopene became widely known as something to eat more of
if you don't want prostate cancer. The scientific world, investigating
details, escalated its efforts to decipher the "lycopene magic." As of this
writing, there now are 1,361(!) scientific publications on lycopene cited
by the National Library of Medicine. 26 A major market is developing,
with trade names like Lycopene 10 Cold Water Dispersion and LycoVit
10% to be used as food supplements. 27 Judging by the health claims,
we might be on the way to bringing prostate cancer, a leading cancer
among men, under control.

There are, though, a couple of disquieting thoughts. First, after
spending millions of research and development dollars, there is some
doubt whether lycopene, as an isolated chemical, can prevent prostate
cancer. According to a more recent publication, six studies now have
shown a statistically significant decrease in prostate cancer risk with
increased lycopene intake; three non-statistically significant studies
agree; and seven studies do not show any association. 28 But these stud-
ies measured lycopene intake from whole foods, namely tomatoes. So,
while these studies certainly indicate that the tomato is still a healthy
food, 28 does that mean we can assume that lycopene, by itself, reduces
prostate cancer risk? There are hundreds, even thousands, of chemicals
in tomatoes. Do we have evidence that isolated lycopene will do what
tomatoes do, especially for those who don't like tomatoes? The answer
is no. 29

There is no evidence for a lycopene-specific effect on prostate cancer,
and I seriously doubt whether we will ever have convincing evidence.
Nonetheless the lycopene business is up and running. In-depth studies
are underway to determine the most effective dose of lycopene as well
as to determine whether commercial lycopene preparations are safe
(when tested in rats and rabbits, that is). 27 Also, consideration is being
given to the possibility of genetically modifying plants for higher levels
of lycopene and other carotenoids. 30 It is a real stretch to call this series
of lycopene reports legitimate science. In my book, this is what I call
technological tinkering and marketing, not science.

Five years before the latest "discovery" of lycopene, a graduate stu-
dent of mine, Youping He, compared four different carotenoids (beta-
carotene, lycopene from tomatoes, canthaxanthin from carrots and
cryptoxanthin from oranges) regarding their ability to prevent cancer in
experimental animals. 3132 Depending on what we were testing and how

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we did the test, single carotenoids could have widely ranging potencies.
While one carotenoid is potent in one reaction, the same carotenoid is
far less potent for another reaction. This variation manifests itself in
countless ways involving hundreds of antioxidants and thousands of
different reactions, forming a nearly indecipherable network. Consum-
ing one carotenoid at a time in the form of a pill will never be the same
as eating the whole food, which provides the natural network of health-
supporting nutrients.

Five years after our rather obscure work on these antioxidants, 32 a
Harvard study 33 effectively kicked off the lycopene campaign. In my
opinion, lycopene, as a cancer fighter, is headed for an already over-
crowded magic bullet graveyard, leaving behind a trail of deep confu-
sion.

FRUIT CLAIMS

The fruit industry plays this game just like everyone else. For example,
when you think of vitamin C, what food product comes to mind? If you
don't think of oranges and orange juice, you are unusual. Most of us
have heard ad nauseum that oranges are a good source of vitamin C.

This belief, however, is just another result of good marketing. How
much do you know, for example, about vitamin C's relationship to diet
and disease? Let's start with the basics. Although you probably know
that oranges are a good source of vitamin C, you may be surprised to
know that many other plant foods have considerably more. One cup of
peppers, strawberries, broccoli or peas all have more. One papaya has as
much as four times more vitamin C than one orange. 34

Beyond the fact that many other foods are better sources of vitamin
C, what can we say about the vitamin C that is in oranges? This con-
cerns the ability of the vitamin to act as an antioxidant. How much of
the total antioxidant activity in an orange is actually contributed by its
vitamin C? Probably not more than l-2%. 35 Furthermore, measuring
antioxidant activity by using "test tube" studies does not represent the
same vitamin C activity that takes place in our bodies.

Most of our impressions about vitamin C and oranges are a mixture
of conjectures and assumptions about out-of-context evidence. Who
first established these assumptions? Orange merchants. Did they jus-
tify their assumptions on the basis of careful research? Of course not.
Did these assumptions (presented as fact) sound good to the marketing
people? Of course they did. Would I eat an orange to get my vitamin

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303

C? No. Would I eat an orange because it is a healthy plant food with a
complex network of chemicals that almost certainly offer health ben-
efits? Absolutely.

I played a small role in this story a couple of decades ago. In the
1970s and 1980s, I appeared in a television ad for citrus fruits. A New
York public relations firm for the Florida Citrus Commission had ear-
lier interviewed me about fruit, nutrition and health. This interview,
unknown to me at the time, was the source of my presence on the ad.
I had not seen the ad and I did not get paid for it, but, nonetheless, I
was one of the talking heads that helped the Florida Citrus Commission
build its case for the vitamin C content of oranges. Why did I do the in-
terview? At that point in my career, I probably thought that the vitamin
C in oranges was important, and, regardless of vitamin C, oranges were
very healthy foods to eat.

It is very easy for scientists to get caught in the reductionism web of
thinking, even if they have other intentions. It has not been until recent-
ly, after a lifetime of research, that I have come to realize how damaging
it is to take details out of context and to make subsequent claims about
diet and health. Industry uses these details extremely well, and the re-
sult is public confusion. Every year, it seems, some new product is being
touted as the key to good health. The situation is so bad that "health"
sections of grocery stores are often stocked more with supplements and
special preparations of seemingly magic ingredients than they are with
real food. Don't be tricked: the healthiest section of any store is the place
where they sell whole fruits and vegetables — the produce section.

Perhaps worst of all, industry corrupts scientific evidence even when
its product has been linked to serious health problems. Our kids are of-
ten the most coveted targets of their marketing. The American govern-
ment has passed legislation preventing cigarette and alcohol companies
from marketing their products to children. Why have we ignored food?
Even though it is accepted that food plays a major role in many chronic
diseases, we allow food industries not only to market directly to chil-
dren, but also to use our publicly-funded school systems to do it. The
long-term burden of our short-sighted indiscretion is incalculable.

Government:
Is It for the People?

During the past two to three decades, we have acquired substantial evi-
dence that most chronic diseases in America can be partially attributed
to bad nutrition. Expert government panels have said it, the surgeon
general has said it and academic scientists have said it. More people die
because of the way they eat than by tobacco use, accidents or any other
lifestyle or environmental factor. We know that the incidence of obe-
sity and diabetes is skyrocketing and that Americans' health is slipping
away, and we know what to blame: diet. So shouldn't the government be
leading us to better nutrition? There is nothing better the government
could do that would prevent more pain and suffering in this country
than telling Americans unequivocally to eat less animal products, less
highly-refined plant products and more whole, plant-based foods. It is a
message soundly based on the breadth and depth of scientific evidence,
and the government could make this clear, as it did with cigarettes.
Cigarettes kill, and so do these bad foods. But instead of doing this, the
government is saying that animal products, dairy and meat, refined sugar
and fat in your diet are good for you! The government is turning a blind
eye to the evidence as well as to the millions of Americans who suffer
from nutrition-related illnesses. The covenant of trust between the U.S.
government and the American citizen has been broken. The United

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States government is not only failing to put out our fires, it is actively
fanning the flames.

DIETARY RANGES: THE LATEST ASSAULT

The Food and Nutrition Board (FNB), as part of the Institute of Medi-
cine (IOM) of the National Academy of Sciences, has the responsibility
every five years or so to review and update the recommended consump-
tion of individual nutrients. The FNB has been making nutrient recom-
mendations since 1943 when it established a plan for the U.S. Armed
Forces wherein it recommended daily allowances (RDAs) for each indi-
vidual nutrient.

In the most recent FNB report, 1 published in 2002, nutrient rec-
ommendations are presented as ranges instead of single numbers, as
was the practice until 2002. For good health, we are now advised to
consume from 45% to 65% of our calories as carbohydrates. There are
ranges for fat and protein as well.

A few quotes from the news release announcing this massive 900+
page report say it all. Here is the first sentence in the news release 2 :

To meet the body's daily energy and nutritional needs while mini-
mizing risk for chronic disease, adults should get 45% to 65% of
their calories from carbohydrates, 20% to 35% from fat and 10% to
35% from protein

Further, we find:

. . . added sugars should comprise no more than 25% of total calo-
ries consumed added sugars are those incorporated into foods

and beverages during production [and] major sources include
candy, soft drinks, fruit drinks, pastries and other sweets. 2

Let's take a closer look. What are these recommendations really say-
ing? Remember, the news release starts off by stating the report's objec-
tive of "minimizing risk for chronic disease." 2 This report says that we
can consume a diet containing up to 35% of calories as fat; this is up
from the 30% limit of previous reports. It also recommends that we can
consume up to 35% of calories as protein; this number is far higher than
the suggestion of any other responsible authority.

The last recommendation puts the frosting on the cake, so to speak.
We can consume up to 25% of calories as added sugars. Remember,
sugars are the most refined type of carbohydrates. In effect, although

GOVERNMENT: IS IT FOR THE PEOPLE?

307

the report advises that we need a minimum of 45% of calories as car-
bohydrates, more than half of this amount (i.e., 25%) can be the sugars
present in candies, soft drinks and pastries. The critical assumption of
this report is this: the American diet is not only the best there is, but
you should now feel free to eat an even richer diet and still be confident
that you are "minimizing risk for chronic disease." Forget any words of
caution you may find in this report — with such a range of possibilities,
virtually any diet can be advocated as minimizing disease risk.

You may have trouble getting your mind around what these figures
mean in everyday terms, so I have prepared the following menu plan that
supplies nutrients in accordance with these guidelines (Chart 16.1). 3 ^

CHART 16.1: SAMPLE MENU THAT FITS INTO THE
ACCEPTABLE NUTRIENT RANGES

Meal

Foods

Breakfast

1 cup Froot Loops
1 cup skim milk

1 package M&M milk chocolate candies
Fiber and vitamin supplements

Lunch

Grilled cheddar cheeseburger

Dinner

3 slices pepperoni pizza, 1 1 6 oz. soda,
1 serving Archway sugar cookies

CHART 16.2: NUTRIENT PROFILE OF SAMPLE MENU PLAN AND
REPORT RECOMMENDATIONS

Nutrient

Sample Menu
Content

Recommended
Ranges

Total Calories

-1800

Varies by height/
weight

Protein (% of total calories)

-18%

10-35%

Fat (% of total calories)

-31%

20-35%

Carbohydrates (% of total calories)

-51%

45-65%

Sugars in Sweets, or Added Sugars
(% of total calories)

-23%

Up to 25%

Folks, I'm not kidding. This disastrous menu plan fits the recommen-
dations of the report and is supposedly consistent with "minimizing
chronic disease."

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What's amazing is that I could put together a variety of menus, all
drenched in animal foods and added sugars, that conform to these rec-
ommended daily allowances. At this point in the book, I don't need to
tell you that when we eat a diet like this day in and day out, we will be
not just marching, but sprinting into the arms of chronic disease. In sad
fact, this is what a large proportion of our population already does.

PROTEIN

Perhaps the most shocking figure is the upper limit on protein intake.
Relative to total calorie intake, only 5-6% dietary protein is required
to replace the protein regularly excreted by the body (as amino acids).
About 9-10% protein, however, is the amount that has been recom-
mended for the past fifty years to be assured that most people at least get
their 5-6% "requirement." This 9-10% recommendation is equivalent
to the well-known recommended daily allowance, or RDA. 5

Almost all Americans exceed this 9-10% recommendation; we con-
sume protein within the range of about 11-21%, with an average of about
15-16%. 6 The relatively few people consuming more than 21% protein
mostly are those who "pump iron," recently joined by those on high-pro-
tein diets.

It is extremely puzzling that these new government-sponsored 2002
FNB recommendations now say that we should be able to consume
protein up to the extraordinary level of 35% as a means of minimizing
chronic diseases like cancer and heart disease. This is an unbelievable
travesty, considering the scientific evidence. The evidence presented
in this book shows that increasing dietary protein within the range of
about 10-20% is associated with a broad array of health problems, espe-
cially when most of the protein is from animal sources.

As reviewed earlier in this book, diets with more animal-based
protein will create higher blood cholesterol levels and higher risks of
atherosclerosis, cancer, osteoporosis, Alzheimer's disease and kidney
stones, to name just a few chronic diseases that the FNB committee
mysteriously chooses to ignore.

Furthermore, the FNB panel had the audacity to say that this 10-35%
recommendation range is the same as previous reports. Their press re-
lease clearly states, "protein intake recommendations are the same [as
previous reports]." I know of no report that has even remotely suggested a
level as high as this.

When I initially saw this protein recommendation, 1 honestly thought

GOVERNMENT: IS IT FOR THE PEOPLE?

309

that it was a printing error. But, no, it was correct. I know several of the
people on the panel who wrote this report and decided to give them a
ring. The first panel member, a long-time acquaintance, said this was
the first time he had even heard about the 35% protein limit! He sug-
gested that this protein recommendation might have been drafted in the
last days of preparing the report. He also told me that there was little
discussion of the evidence on protein, for or against a high consump-
tion level, although he recollected there being some pro-Atkins sympa-
thy on the committee. He had not worked in the protein area, so he did
not know the literature. In any event, this important recommendation
slipped through the panel without much notice and made the first sen-
tence of the FNB news release!

The second panel member, a long-time friend and colleague, was a
subcommittee chair during the latter part of the panel's existence. He is
not a nutritional scientist and also was surprised to hear my concerns
about the upper limit for protein. He did not recall much discussion
on the topic either. When I reminded him of some of the evidence
linking high-animal protein diets to chronic disease, he initially was
a little defensive. But with a little more persistence on my part about
the evidence, he finally said, "Colin, you know that I really don't know
anything about nutrition." How, then, was he a member — let alone the
chair — of this important subcommittee? And it gets worse. The chair of
the standing committee on the evaluation of these recommendations
left the panel shortly before its completion for a senior executive posi-
tion in a very large food company — a company that will salivate over
these new recommendations.

A SUGARCOATED REPORT

The recommendation on added sugar is as outrageous as the one for
protein. At about the time this FNB report was being released, an expert
panel put together by the WHO (World Health Organization) and the
FAO (Food and Agriculture Organization) was completing a new report
on diet, nutrition and the prevention of chronic diseases. Professor
Phillip James, another friend of mine, was a member of this panel and a
panel spokesperson on the added sugar recommendation. Early rumors
of the report's findings indicated that the WHO/FAO was on the verge
of recommending an upper safe limit of 10% for added sugar, far lower
than the 25% established by the American FNB group.

Politics, however, had early entered the discussion, as it had done in

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earlier reports on added sugars. 7 According to a news release from the
director-general's office at the WHO, 8 the U.S. -based Sugar Association
and the World Sugar Research Organization, who "represent the inter-
ests of the sugar growers and refiners, had mounted a strong lobbying
campaign in an attempt to discredit the [WHO] report and suppress its
release." They did not like setting the upper safe limit so low. Accord-
ing to the Guardian newspaper of London, 7 the U.S. sugar industry was
threatening "to bring the World Health Organization to its knees" un-
less it abandoned these guidelines on added sugar. WHO people were
describing the threat "as tantamount to blackmail and worse than any
pressure exerted by the tobacco industry." 7 The U.S.-based group even
publicly threatened to lobby the U.S. Congress to reduce the $406 mil-
lion U.S. funding of the WHO if it persisted in keeping the upper limit
so low at 10%! There were reports, after a letter was sent by the industry
to Secretary of Health and Human Services Tommy Thompson, that the
Bush administration was inclined to side with the sugar industry. I, and
many other scientists, were being encouraged at that time to contact
our congressional representatives to stop this outrageous strong-armed
tactic by the U.S. sugar companies.

So, for added sugars, we now have two different upper "safe" lim-
its: a 10% limit for the international community and a 25% limit for
the U.S. Why such a huge difference? Did the sugar industry succeed
in controlling the U.S.-based FNB report but fail with the WHO/FAO
report? What does this say about the FNB scientists who also devised
the new protein recommendation? These wildly different estimates are
not a matter of scientific interpretation. This is nothing more than na-
ked political muscle. Professor James and his colleagues at the WHO
stood up to the pressure; the FNB group appears to have caved in. The
U.S. panel received funding from the M&M Mars candy company and
a consortium of soft drink companies. Is it possible that the U.S. group
felt an obligation to these sugar companies? Incidentally, the sugar in-
dustry, in their fight against the WHO conclusion, has relied heavily 7 on
the FNB report with its 25% limit. In other words, the FNB committee
produces a friendly recommendation for the sugar industry which then
turns around and uses this finding to support its claim against the WHO
report.

GOVERNMENT: IS IT FOR THE PEOPLE?

311

THE INFLUENCE OF INDUSTRY

This discussion still leaves unanswered the question of how industry
develops such extraordinary influence. Mostly, industry develops con-
sultancies with a few publicly visible figures in academia, who then take
leadership in policy positions outside of academia. However, these in-
dustry consultants continue to wear their academic hats. They organize
symposia and workshops, write commissioned reviews, chair expert
policy groups and/or become officers of key professional societies. They
gravitate toward the leadership positions in science-based organizations
that develop significant policy and publicity.

Once in these positions, these people then have the opportunity
to assemble teams to their liking, by choosing committee members,
symposia speakers, management staff, etc. The kinds of people most
helpful to the team are either colleagues with similar prejudices and/or
colleagues who are oblivious to who is "calling the shots." It's called
"stacking the deck," and it really works.

In the case of the FNB, its panel was organized while under the chair-
manship of an academic who had strong personal ties with the dairy
industry. He helped in selecting the "right" people and helped in setting
the agenda for the report, the most significant roles that anyone could
have played. Is it surprising that the dairy industry, which must be ec-
static with the panel's findings, also helped to finance the report?

You might be surprised to learn that academic scientists can receive
personal compensation from industry while simultaneously undertak-
ing government-sponsored activities of considerable public importance.
Ironically, they can even help set the agenda for the same government
authorities who have long been restricted from such corporate associa-
tions. It is a huge "conflict-of-interest" loophole allowing industries to
exercise their influence through the side door of academia. In effect, the
entire system is essentially under the control of industry. The govern-
ment and academic communities, playing their respective roles, mostly
do as they are expected to do.

In addition to M&M Mars company, the corporate sponsors of the
FNB report also included major food and drug companies that would
benefit from higher protein and sugar allowances. 2 The Dannon Insti-
tute, a leading dairy-based consortium promoting its own brand of nu-
trition information, and the International Life Sciences Institute (ILSI),
which is a front group for about fifty food, supplement and drug compa-

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nies, both contributed funding for the FNB report. Corporate members
include Coca-Cola, Taco Bell, Burger King, Nestle, Pfizer and Roche
Vitamins. 9 Some drug companies sponsored the report directly, in addi-
tion to their support through the International Life Sciences Institute. I
don't recall private corporations providing financial support for the NAS
expert panels that I served on.

It seems as if there is no end to this story. The chair of the FNB has
been an important consultant to several major dairy-related companies
(e.g., National Dairy Council, Mead Johnson Nutritionals, which is
a major seller of dairy-based products, Nestle Company and a Dan-
non yogurt affiliate). 10 Simultaneously, he was chair of the Dietary
Guidelines Committee that establishes the Food Guide Pyramid and
sets national nutrition policy affecting the National School Lunch and
Breakfast programs, the Food Stamp Program and the Women, Infants
and Children Supplemental Feeding Program (WIC). 1, 10 As chair of this
latter committee, his personal financial associations with the food in-
dustry were not publicly revealed as required by federal law. 11 Eventual-
ly a court order, initiated by the Physician's Committee for Responsible
Medicine, 12 was required to force him and his fellow colleagues to reveal
their relationships with the food industry. Although the chair's industry
associations were more substantial, six of the eleven committee members
also were shown to have ties to the dairy industry. 10 - 11

The entire system of developing public nutrition information, as I
originally saw with the Public Nutrition Information Committee that
I once chaired (see chapter eleven), has been invaded and co-opted by
industry sources that have the interest and resources to do so. They run
the show. They buy a few academic hacks who have gained positions of
power and who exercise considerable influence, both within academia
and government.

It seems curious that while government scientists are not allowed
to receive personal compensation from the private sector, their col-
leagues in academia can receive all that they can get. In turn, these
conflicted individuals then run the show in collaboration with their
government counterparts. However, restricting academics from receiv-
ing corporate consultancies is not the answer. That would only drive
it underground. Rather, the situation would be best handled by mak-
ing one's industry connections a matter of public disclosure. Everyone
needs to know the full extent of each academic's associations with
the private sector. Disclosure and full transparency is in everyone's

GOVERNMENT: IS IT FOR THE PEOPLE?

313

interest. These associations should not be something we have to go to
court to discover.

SETTING US BACK FOR YEARS

Lest you think that this Food and Nutrition Board report is merely a
five-second news bite that then gets filed into a dusty old cabinet some-
where in Washington, let me assure you that tens of millions of people
are directly affected by this panel's findings. According to the summary
of the report itself, 13 the recommended levels of nutrient consumption
that are set by this panel are

the basis for nutrition labeling of foods, for the Food Guide Pyra-
mid and for other nutrition education programs . . . [They are]
used to determine the types and amounts of food:

• provided in the WIC (Women, Infants and Children) Supple-
mental Feeding Program and the Child Nutrition Programs
such as School Lunch,

• served in hospitals and nursing homes for Medicare reim-
bursement,

• found in the food supply that should be fortified with specific
nutrients,

• used in a host of other important federal and state programs
and activities [such as establishing reference values used in
food labeling] 13

The School Lunch Program feeds 28 million children every day With
officially recommended consumption patterns like these, we are at liberty
to put any agricultural commodity we want into the hungry mouths of
children already suffering from unprecedented levels of obesity and dia-
betes. By the way, the 2002 FNB report does make one special exception
for children: it says that they can consume up to 40% of calories as fat, up
from 35% for the rest of us, while minimizing the risk of chronic disease.
The Women, Infants and Children Program affects the diets of another 7
million Americans, and the Medicare hospital programs feed millions of
people every year. It is safe to say that the food provided by these govern-
ment programs directly feeds at least 35 million Americans a month.

For people who are not directly fed by the government, this nutri-
ent information still has significant consequences. From September
2002 onwards, nutrition education programs around the country

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have incorporated these new guidelines. This includes education in
primary schools, universities, health professional programs and other
community-based programs. Food labels also will be affected by these
changes, as will the nutrition information that seeps into our lives via
advertising.

Almost all of the wide-ranging effects of this 2002 FNB report will be
profoundly harmful. In school, our children can be fed more fat, more
meat, more milk, more animal protein and more sugar. They will also
learn that this food is consistent with good health. The ramifications
of this are serious, as a whole generation will walk the path of obesity
diabetes and other chronic illnesses, all the while believing that they
are doing the right thing. Meanwhile, our government and its academic
hacks can feel free to unload more meat, more fat, more animal protein
and more sugar onto the neediest among us (e.g., the Women, Infants
and Children (WIC) participants). I consider this to be an irresponsible
and callous disregard for American citizens. Of course, these women
and infants are not in a position to pay for research, donate to politi-
cians, give academics special favors or fund government panels! For
others concerned about nutrition, every time they see a dietitian, every
time they see their doctor, every time they see a nutritionist and every
time they go to a community health center, they may be told that a
diet high in fat, animal protein, meat and dairy is consistent with good
health, and they needn't worry about eating too many sweets. Posters
that deck the bulletin boards of public institutions will now feature
these new government guidelines as well.

In short, this 2002 FNB report, which represents the most sweeping,
regressive nutrition policy statement I have ever seen, will either indi-
rectly or directly promote sickness among Americans for many years to
come. Having been a member of several diet and health policy-making
expert panels over a twenty-year period I harbored the view that these
panels were dedicated to the promotion of consumer health. I no longer
believe this to be true.

UNFUNDED NUTRITION

Not only is the government failing to promote health through its recom-
mendations and reports, it is squandering an opportunity to promote
public health through scientific research. The U.S. National Institutes
of Health (NIH) is responsible for funding at least 80-90% of all bio-
medical and nutrition-related research that is published in the scientific

GOVERNMENT: IS IT FOR THE PEOPLE?

315

literature. To address various health topics, the NIH is comprised of
twenty-seven separate institutes and centers, including its two largest,
the National Cancer Institute (NCI) and the National Heart, Lung and
Blood Institute. 14 With a proposed 2005 budget of almost $29 billion, 15
the NIH is the center of the government's gigantic medical research ef-
forts.

In terms of nutrition research, however, something is amiss. None
of these twenty-seven institutes and centers at the NIH is devoted to
nutrition, despite the pivotal nature of nutrition in health, and despite
the public interest in the subject. One of the arguments against having a
separate institute for nutrition is that the existing institutes already con-
cern themselves with nutrition. But this does not happen. Chart 16.3
shows the funding priorities for various health topics at the NIH. 16

Of the $28 billion NIH budget proposed for 2004, only about 3.6%
is designated for projects that are related in some way to nutrition 17 and
24% for projects that are related to prevention. That may not sound too
bad. But these figures are seriously misleading.

Most of the prevention and nutrition budgets have absolutely noth-
ing to do with prevention and nutrition, as I have written in this book.

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We won't be hearing about exciting research on dietary patterns, nor
will there be serious efforts to tell the public how diet affects health.
Instead, the prevention and nutrition budgets will be designated for
developing drugs and nutrient supplements. A few years ago, the direc-
tor of the NCI, the oldest of the NIH institutes, described prevention
as "efforts to directly prevent and/or inhibit malignant transformation,
to identify, characterize and manipulate factors that might be effective
in achieving that inhibition and attempts to promote preventative mea-
sures." 18 This so-called prevention is all about manipulation of isolated
chemicals. "Identifying, characterizing and manipulating factors" is a
not-so-secret code for drug discovery.

Considered from another perspective, the NCI (of the NIH), in 1999,
had a budget of S2.93 billion. 19 In a "major" 5-A-Day dietary program, it
was spending $500,000 to $1 million to educate the public to consume
five or more servings of fruits and vegetables per day. 18 This is only three
hundredths oj one percent (0.0256%) of its budget. That's $2.56 for every
$10,000! If it calls this a major campaign, I pity its minor campaigns.

The NCI also has been funding a couple of multi-year large studies,
including the Nurses' Health Study at Harvard (discussed in chapter
twelve) and the Women's Health Initiative, mostly devoted to the testing
of hormone replacement therapy vitamin D and calcium supplementa-
tion, and the effect of a moderately low-fat diet on prevention of breast
and colon cancer. These rare nutrition-related studies unfortunately
suffer from the same experimental flaws described in chapter fourteen.
Almost always, these studies are designed to tinker with one nutrient at
a time, among an experimental population that uniformly consumes a
high-risk, animal-based diet. These studies have a very high probability
of creating some very expensive confusion that we hardly need.

If very few of our tax dollars are used to fund nutrition research, what
do they fund? Almost all of the billions of dollars of taxpayer money
expended by the NIH each year funds projects to develop drugs, supple-
ments and mechanical devices. In essence, the vast bulk of biomedical
research funded by you and me is basic research to discover products
that the pharmaceutical industry can develop and market. In 2000, Dr.
Marcia Angell, a former editor of the New England Journal oj Medicine,
summarized it well when she wrote 20 :

. . . the pharmaceutical industry enjoys extraordinary government
protections and subsidies. Much of the early basic research that

GOVERNMENT: IS IT FOR THE PEOPLE?

317

may lead to drug development is funded by the National Institutes
of Health (ref. cited). It is usually only later, when the research
shows practical promise, that the drug companies become in-
volved. The industry also enjoys great tax advantages. Not only are
its research and development costs deductible, but so are its mas-
sive marketing expenses. The average tax rate of major U.S. indus-
tries from 1993 to 1996 was 27.3% of revenues. During the same
period the pharmaceutical industry was reportedly taxed at a rate
of only 16.2% (ref. cited). Most important, the drug companies en-
joy seventeen-year government-granted monopolies on their new
drugs — that is, patent protection. Once a drug is patented, no one
else may sell it, and the drug company is free to charge whatever
the traffic will bear. 20

Our tax dollars are used to make the pharmaceutical industry more
profitable. One could argue that this is justified by gains in public
health, but the alarming fact is that this litany of research into drugs,
genes, devices and technology research will never cure our chronic dis-
eases. Our chronic diseases are largely the result of infinitely complex
assaults on our bodies resulting from eating bad food. No single chemi-
cal intervention will ever equal the power of consuming the healthiest
food. In addition, isolated chemicals in drug form can be very danger-
ous. The National Cancer Institute itself states, "What is clear is that
most of our current treatments will produce some measure of adver-
sity." 21 There is no danger to eating a healthy diet, and there are far
more benefits, including massive cost savings both on the front end of
preventing disease and on the back end of treating disease. So why is
our government ignoring the abundant scientific research supporting
a dietary approach in favor of largely ineffective, potentially dangerous
drug and device interventions?

PERSONAL ACCOUNTS

In terms of public nutrition policy, I want to leave you with one short sto-
ry that says so much about the government's priorities. One of my former
graduate students at Cornell, Antonia Demas (now Dr. Antonia Demas),
did her doctoral research in education by teaching a healthy food-and-nu-
trition-based curriculum 22 to elementary school kids and then integrating
those healthy foods into the school lunch program. She had been doing
this work as a volunteer mother in her children's schools for seventeen

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years prior to her graduate studies. I was her advisor for the nutrition
part of her dissertation research.

The U.S. Department of Agriculture administers the school lunch
program to 28 million children, largely relying on an inventory of gov-
ernment-subsidized foods. The government program, as it now stands,
uses mostly animal-based products and even requires that participating
schools make available cow's milk. At the local level, this usually means
that consumption of milk is mandatory.

Dr. Demas's innovative research on the school lunch program was a
great success; children loved the learning style and were excited to eat
the healthy foods when they went through the lunch line. The children
then convinced their parents to eat the healthy food at home. Dr. Demas's
program won national awards for the "most creative implementation of
the dietary guidelines" and "excellence in nutrition education." The
program has proven to be of interest to more than 300 school lunch and
behavioral rehabilitation programs around the U.S., including schools
in areas as widely dispersed as Hawaii, Florida, Indiana, New England,
California and New Mexico. In this effort, Dr. Demas has organized a
nonprofit foundation (Food Studies Institute, Trumansburg, New York)
and written a curriculum ("Food is Elementary"). And here's the kicker:
Dr. Demas's program is entirely plant-based.

I had the opportunity to go to Washington and talk with Dr. Eileen
Kennedy, who, at the time, was the director of the Center for Nutrition
Policy and Promotion at the USDA. Dr. Kennedy was deeply involved
both in the school lunch program and the dietary guidelines commit-
tee, on which it was revealed that she had ties to the dairy industry. She
is now the Deputy Undersecretary for the USDAs Research, Education
and Economics division. The topic of our discussion was Dr. Demas's
innovative school lunch program and how it was garnering national
attention. At the end of this discussion, I said to her, "You know, that
program is entirely plant-based." She looked at me, wagged her finger as
if I were being a bad boy, and said, "We can't have that."

I have come to the conclusion that when it comes to health, govern-
ment is not for the people; it is for the food industry and the pharmaceu-
tical industry at the expense of the people. It is a systemic problem where
industry, academia and government combine to determine the health
of this country. Industry provides funding for public health reports,
and academic leaders with industry ties play key roles in developing
them. A revolving door exists between government jobs and industry

GOVERNMENT: IS IT FOR THE PEOPLE?

319

jobs, and government research funding goes to the development of
drugs and devices instead of healthy nutrition. It is a system built by
people who play their isolated parts, oftentimes unaware of the top de-
cision makers and their ulterior motivations. The system is a waste of
taxpayer money and is profoundly damaging to our health.

Big Medicine: Whose Health
Are They Protecting?

When is the last time that you went to the doctor and he or she told
you what to eat or what not to eat? You've probably never had that ex-
perience. But the vast majority of Americans will fall prey to one of the
chronic diseases of affluence discussed in Part II, and, as you have seen,
there is a wealth of published research that suggests these diseases are a
result of poor nutrition, not poor genes or bad luck. So why doesn't the
medical system take nutrition seriously?

Four words: money, ego, power and control. While it is unfair to
generalize about individual doctors, it is safe to say that the system they
work in, the system that currently takes responsibility for promoting
the health of Americans, is failing us. No one knows this better than
the tiny minority of doctors who treat their patients from a nutritional
perspective. Two of the most prominent doctors in this minority have
spent many years emphasizing diet and health, both in public within
their profession and in private with their patients. They have had ex-
ceptionally impressive results protecting their patients' health. These
two doctors are Caldwell B. Esselstyn, Jr. , whose work I discussed in
chapter five, and John McDougall, an internist. My son Tom and I sat
down with these men recently to discuss their experience advocating a
whole foods, plant-based diet in the medical setting.

321

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DR. SPROUTS

Long before our country was founded, Dutch pioneers had settled in
the Hudson Valley north of New York City. One of these settler families
were the Esselstyns. They started farming a plot of land in 1675. Nine
generations later, that farm still belongs to the Esselstyn family. Dr. Es-
selstyn and his wife Ann own the several-hundred-acre Hudson Valley
farm, just over two hours north of New York City. They spent the sum-
mer of 2003 living in the country, working the farm, growing a garden,
hosting their kids and grandkids and enjoying a more relaxed life than
what they're used to in Cleveland, Ohio.

Ess and Ann have a modest house: a large, rectangular, converted
storage building. The simplicity of it belies the fact that this is one of
the oldest family farms in America. Only upon closer inspection does
it become apparent that there is something unusual about this place.
Hanging on the wall is a framed certificate from New York State given to
the Esselstyn family in recognition of their family farm, a farm that has
now seen parts of five different centuries. Nearby an oar hangs on the
wall. It is the oar Ess used in 1955 as an oarsman at Yale, when Yale beat
Harvard by five seconds. Ess explains he has three other oars: two from
beating Harvard in other years, and one for winning the gold medal in
the Olympics with the Yale crew in 1956.

Downstairs, there is an exceptionally old photograph of Ess's great
great grandfather on the farm. Around the corner there's an impressive-
looking museum-style schematic of the Esselstyn family tree, and on
the other end of the hall, there's a large black and white picture of Ess's
father standing in front of a microphone, exchanging comments with
John E Kennedy during a White House address. Despite its humble
appearance, it is very clear that this is a place with a distinguished his-
tory.

After touring the farm on a tractor, we sat down with Ess and asked
him about his past. After graduating from Yale, he was trained as a sur-
geon at the Cleveland Clinic and at St. George's Hospital in London.
He remembers fondly some of his most influential mentors: Dr. George
Crile, Jr., Dr. Turnbull and Dr. Brook. Dr. Crile, a giant at the Cleve-
land Clinic, eventually became Ess's father-in-law upon Ess's marriage
to Ann. Dr. Crile was a man of exceptional accomplishment, playing
a courageous, leading role in questioning the macabre surgery called
"radical mastectomy." 1 Dr. Turnbull and Dr. Brook were also renowned

BIG MEDICINE: WHOSE HEALTH ARE THEY PROTECTING?

323

surgeons. In addition, Ess's own father was a distinguished physician
with a national reputation. But, as Ess remembers, despite being "health
experts," all four of these men were "ravaged by cardiovascular dis-
ease." His own father had a heart attack at age forty-two and Dr. Brook
had a heart attack at age fifty-two.

These were the men he looked up to, and when it came to cardiovas-
cular disease, all of them were helpless. Shaking his head, Ess said, "You
can't escape this disease. These people, who were giants in the prime of
their years, just withered." As he took a moment to remember his father,
he said, "It was the last year or two of my dad's life, and we were just
strolling along one day. He was saying, 'We are going to have to show
people how to lead healthier lives.' He was right on it. He was intensely
interested in preventive medicine, but he didn't have any information."
His father's interest has been a driving influence in Ess's life.

Following in these men's footsteps, Ess went on to amass an extraor-
dinarily impressive list of awards and credentials: an Olympic gold
medal in rowing; a Bronze Star for military service in Vietnam; President
of the Staff, member of the Board of Governors, chairman of the Breast
Cancer Task Force, and head of the Section of Thyroid and Parathyroid
Surgery at the Cleveland Clinic, one of the top-ranked medical institu-
tions in the world; president of the American Association of Endocrine
Surgeons; over 100 professional scientific articles; and inclusion on a
list in 1994-95 of the best doctors in America. 2 He remembers, "For
about a ten- to fifteen-year period I was the top earner in the depart-
ment of general surgery. As Dr. Crile's son-in-law, I was panicked about
not pulling my weight. I didn't get home until late at night, but I had
a position that was secure." When the then-president of the American
Medical Association needed thyroid surgery, he wanted Ess to be the
one to operate.

But despite the accolades, the titles and the awards, something was
not right. So often, Ess's patients did not regain their health, even after his
best efforts. As Ess described it, he had "this haunting feeling that was
really beginning to bother me. I kept looking at how the patients were
doing after these operations." Slightly exasperated, he said, "What is
the survival rate for cancer of the colon? It's not so great!" He recounted
the operation for colon cancer on one of his best friends. During sur-
gery, they saw that the cancer had spread throughout the intestines. Ess
lowered his voice ever so slightly in remembering this, saying, "You get
there after the horse has left the barn." In thinking about all the breast

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surgery he had done, the lumpectomies and mastectomies, he expressed
disgust at the idea of "disfiguring somebody when you know that you
haven't changed their chances for recovery."

He began to do some soul searching. "What is my epitaph going to
be? Five thousand mastectomies! You've disfigured more women than
anybody else in Ohio!" Dropping the sarcasm, he said with sincerity, "I
think everybody likes to leave the planet thinking that maybe . . . maybe
you've helped a little."

Dr. Esselstyn began studying the literature on the diseases he com-
monly treated. He read some of the popular work of Dr. John McDou-
gall, who had just written a best-selling diet and health book called The
McDougall Plan. 3 He read the scientific literature that compared inter-
national disease rates and lifestyle choices, and a study by a University
of Chicago pathologist showing that a low-fat, low-cholesterol diet fed
to nonhuman primates could reverse atherosclerosis. He came to the
realization that the diseases that so often plagued his patients were due
to a diet rich in meat, fat and highly refined foods.

As mentioned in chapter five, he got the idea to treat heart patients
with a low-fat, plant-based diet, and in 1985 went to the head of the
Cleveland Clinic to discuss his study. She said that nobody had ever
shown that heart disease in humans could be reversed by using dietary
treatment. Still, Ess knew he was on the right track and went about qui-
etly conducting his study over the next several years. The study he pub-
lished, of eighteen patients with heart disease, demonstrated the most
dramatic reversal of heart disease in the history of medicine, simply by
using a low-fat, plant-based diet and a minimal amount of cholesterol-
reducing medication.

Esselstyn has become a champion of dietary treatment of disease, and
he has the data to prove his case. But it hasn't been easy. Rather than
recognizing him as a hero, some in the medical establishment would
rather he disappear. Somewhere in this transition from top-ranked,
self-described "macho, hard-ass surgeon" to dietary advocate, he has
become known, behind his back, as Dr. Sprouts.

A DAUNTING TASK

What's interesting about this story is that a man who had reached the
pinnacle of a highly respected profession dared to try something dif-
ferent, succeeded, and then quickly found himself on the outside of

BIG MEDICINE: WHOSE HEALTH ARE THEY PROTECTING? 325

the establishment looking in. He had threatened the status quo by his
circumvention of standard treatments.

Some of Ess's colleagues have disparaged his treatment as being too
"extreme." Some doctors have dismissed it by saying, "I think the re-
search in this area is pretty soft," which is an absurd comment consider-
ing the breadth and depth of the international studies, the animal stud-
ies and the intervention studies. Some doctors have said to Ess, "Yeah
okay, but nobody is going to eat like that. I can't even get my patients
to stop smoking." Ess's response was, "Well, you really have no training
in this. This requires just as much expertise as doing a bypass. It takes
three hours for me to counsel a patient," not to mention the diligence
required for the constant follow-up and monitoring of the patient's
health. One patient told his cardiologist that he wanted to see Ess and
commit to a dietary program to reverse his heart disease. The cardiolo-
gist responded, "Now you listen to me. There is no way to reverse this
disease." You'd think that doctors would be more excited about healing
their patients!

In talking about doctors and their unwillingness to embrace a whole
foods, plant-based diet, Ess says, "You can't get frustrated. These aren't
evil people. There are sixty cardiologists [at the Cleveland Clinic], any
number of whom are closet believers in what I do, but they're a little
afraid because of the power structure."

For Ess, however, it has been impossible to avoid his share of frustra-
tion. Early on, when he was first suggesting dietary treatment of heart
disease, colleagues greeted the idea with caution. Ess figured that their
attitude was born out of the fact that scientific research showing effec-
tive dietary intervention of heart disease in humans wasn't yet strong
enough. But later, scientific results of unparalleled success, including
Esselstyn's, were published. The data have been strong, consistent and
deep, yet Ess still encountered reluctance to embrace this idea:

You take a cardiologist and he's learned all about beta blockers, he's
learned about calcium antagonists, he's learned about how to run
this catheter up into your heart and blow up balloons or laser it or
stent it without killing you and it's very sophisticated. And there's all
these nurses and there's lights out and there's drama. I mean it's just,
oh my god, the doctor blows up the balloon in his head. The ego of
these people is enormous. And then someone comes along and says,
"You know, I think we can cure this with brussels sprouts and broc-

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coli." The doctor's response is, "WHAT? I learned all this crap, I'm
making a freakin' fortune, and you want to take it all away?"

Then when that person comes along and actually cures patients with
brussels sprouts and broccoli, as Esselstyn did, and gets better results
than any other pill or procedure known, you've suddenly announced
that something works, hands down, better than what 99% of the profes-
sion is doing. Summarizing his point, Ess says:

Cardiologists are supposed to be expert in diseases of the heart —
and yet they have no expertise in treating heart disease, and when
that awareness strikes them, they get very defensive. They can
treat the symptoms, they can take care of arrythmias, they can get
you interventions, but they don't know how to treat the disease,

which is a nutritional treatment Imagine a dietitian training a

heart surgeon!

Esselstyn has found that merely saying that patients can have control
over their own health is a challenge to many. These experts, after all,
are built up to be the dispensers of health and healing. "Intellectually
it's very challenging to think that the patient can do this with greater
alacrity, dispatch, safety, and it's something that's going to endure." With
all of the doctor's gadgets, technologies, training and knowledge, noth-
ing is more effective than guiding the patient to make the right lifestyle
choices.

But Ess is quick to point out that doctors are not malicious people
engaged in a conspiracy:

The only person that likes change is a newborn, and it's natural,
it's human nature. Anywhere you go, 99% of the people are eating
incorrectly. The numbers are against you, and it's very hard for
those 99% to look at you in the 1% and say, "Yes, he's right, we are
all wrong."

Another obstacle: lack of nutrition knowledge amongst physicians.
Ess has had his share of interaction with ignorant doctors, and his im-
pression is that "it's absolutely daunting, the lack of physician knowl-
edge that there is about the fact that disease can be reversed. You won-
der, what is the literature that these guys read?"

Physician knowledge often involves only the standard treatments:
pills and procedures. "What does the twentieth century of medicine

BIG MEDICINE: WHOSE HEALTH ARE THEY PROTECTING?

327

have to offer? We have pills and we have procedures. Right?" Esselstyn
leans forward and, with a slight grin, as if he's about to tell us the em-
peror has no clothes, he says, "But who ever says, 'Maybe we ought to stop
disease'?" In Dr. Esselstyn's experience, stopping disease does not figure
prominently into the status quo.

LACK OF TRAINING

The medical status quo relies heavily on medication and surgery, at the
exclusion of nutrition and lifestyle. Doctors have virtually no training in
nutrition and how it relates to health. In 1985 the United States National
Research Council funded an expert panel report that investigated the
quantity and quality of nutrition education in U.S. medical schools/
The committee's findings were clear: "The committee concluded that
nutrition education programs in U.S. medical schools are largely inad-
equate to meet the present and future demands of the medical profes-
sion." 4 But this finding was nothing new. The committee noted that
in 1961 the "American Medical Association Council on Foods and
Nutrition reported that nutrition in the U.S. medical schools received
'inadequate recognition, support and attention.'" 4 ' 5 In other words, over
forty years ago, the doctors themselves said that their nutrition training
was inadequate. Nothing had changed by 1985, and up to the present
time, articles continue to be written documenting the lack of nutrition
training in medical schools. 6, 7

This situation is dangerous. Nutrition training of doctors is not merely
inadequate; it is practically nonexistent. In 1985, the National Research
Council report found that physicians receive, on average, only twenty-
one classroom hours (about two credits) of nutrition training during
their four years of medical school. 4 The majority of the schools surveyed
actually taught less than twenty contact hours of nutrition, or one to
two credit hours. By comparison, an undergraduate nutrition major at
Cornell will receive twenty-five to forty credit hours of instruction, or
about 250-500 contact hours; registered dietitians will have more than
500 contact hours.

It gets worse. The bulk of these nutrition hours are taught in the first
year of medical school, as part of other basic science courses. Topics
covered in a basic biochemistry course may include nutrient metabo-
lism and/or biochemical reactions involving certain vitamins or miner-
als. In other words, nutrition is often not taught in relation to public health
problems, like obesity, cancer, diabetes, etc. In conjunction with the 1985

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government report, the president of the American Medical Students As-
sociation, William Kassler, writes 8 :

Most nutrition in the formal curriculum is incorporated into
other courses. Biochemistry, physiology and pharmacology are the
courses most often alleged to contain some nutrition instruction.
Too often in such courses, nutrition is touched on briefly, with the
primary emphasis on the major discipline. It is quite possible to fin-
ish such a course and not even realize that nutrition was covered [my
emphasis]. Nutrition taught by those whose interest and expertise
lie elsewhere simply doesn't work.

It gets even worse! When nutrition education is provided in rela-
tion to public health problems, guess who is supplying the "educa-
tional" material? The Dannon Institute, Egg Nutrition Board, National
Cattlemen's Beef Association, National Dairy Council, Nestle Clinical
Nutrition, Wyeth-Ayerst Laboratories, Bristol-Myers Squibb Company,
Baxter Healthcare Corporation and others have all joined forces to
produce a Nutrition in Medicine program and the Medical Nutrition
Curriculum Initiative. 9 ' 10 Do you think that this all-star team of animal
foods and drug industries representatives is going to objectively judge
and promote optimal nutrition, which science has shown to be a whole
foods, plant-based diet that minimizes the need for drugs? Or might
they try to protect the meat-centered, Western diet where everyone
expects to pop a pill for every sickness? This organization is creating
nutrition curricula, involving CD-ROMS, and giving them away to
medical schools for free. As of late 2003, 112 medical schools were
using the curriculum. 11 According to their Web site, "Plans are un-
derway for developing versions for undergraduate nutrition students,
continuing medical education and other health professions audiences."
(http://www.med.unc.edU/nutr/nim/FAQ.htm#anchorl97343)

The dairy industry has also funded research investigations into nu-
trition education in medical schools 12 and has funded "prestigious"
awards. 13 ' 14 These efforts show that industry is well prepared to promote
its monetary interests whenever the opportunity presents itself.

You should not assume that your doctor has any more knowledge
about food and its relation to health than your neighbors and cowork-
ers. It's a situation in which nutritionally untrained doctors prescribe
milk and sugar-based meal-replacement shakes for overweight diabet-
ics, high-meat, high-fat diets for patients who ask how to lose weight

BIG MEDICINE: WHOSE HEALTH ARE THEY PROTECTING?

329

and extra milk for patients who have osteoporosis. The health damage
that results from doctors' ignorance of nutrition is astounding.

Apparently, there aren't enough "nutrition-oriented physician role
models" in medical education. A recent survey found "a shortage of nu-
trition-oriented physician role models is probably the major constraint in
teaching nutrition to residents." 12 I suspect that these medical programs
lack nutrition-oriented physicians simply because they do not make it a
priority to hire them. Nobody knows this better than Dr. John McDou-
gall.

DR. MCDOUGALL'S CHALLENGE

Dr. John McDougall has been advocating a whole foods, plant-based ap-
proach to health longer than any practitioner I know. He has written ten
books, including several that have sold over a half a million copies each.
His nutrition and health knowledge is phenomenal, greater than any oth-
er doctor I've met and greater than any of my nutrition colleagues in aca-
demia. We met recently in his Northern California home, and one of the
first things he showed me was his bank of four or five full- size metal file
cabinets lined up along the back of his study. There can't be many people
in the country with a collection of scientific literature on diet and disease
that could rival John McDougall's, and, most importantly, John maintains
a high level of familiarity with all of it. It is not unusual for him to spend a
couple of hours a day on the Internet reviewing the latest journal articles.
If anybody would be a perfect "nutrition-oriented physician role model"
in an educational setting, it would be Dr. John McDougall.

Growing up, John ate a rich, Western diet. As he says, he had four
feasts a day: Easter during breakfast, Thanksgiving at lunch, Christmas
at dinner and a birthday party for dessert. It caught up to him, and at the
age of eighteen, a few months into college, John had a stroke. After re-
covering with a new appreciation for life, he became a straight A student
as an undergraduate and then completed medical school in Michigan
and an internship in Hawaii. He chose to practice on the Big Island of
Hawaii, where he cared for thousands of patients, some of whom had
recently migrated from China or the Philippines, and some who were
fourth generation Chinese or Filipino Americans.

It was there that John became an unhappy doctor. Many of his pa-
tients' health problems were a result of chronic illnesses, such as obesity
diabetes, cancer, heart disease and arthritis. John would treat them as
he was taught, with the standard sets of pills and procedures, but very

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few of them became healthy. Their chronic diseases didn't go away, and
John quickly realized that he had severe limitations as a doctor. He also
started to learn something else from his patients: the first and second
generation Americans from Asia, the ones who ate more traditional,
Asian staple diets of rice and vegetables, were trim, fit and not afflicted
with the chronic diseases that plagued John's other patients. The third
and fourth generation Asian Americans, however, had fully adopted
America's eating habits and suffered from obesity, diabetes and the
whole host of other chronic diseases. It was from these people that John
began to notice how important diet was for health.

Because John wasn't healing people, and the pills and procedures
weren't working, he decided he needed more education and entered a
graduate medical program (residency) at the Queens Medical Center in
Honolulu. It was there that he began to understand the boundaries that
the medical establishment had set and the way that medical education
molds the way doctors are supposed to think.

John went into the program hoping to find out how to perfect the
pills and procedures so that he could become a better doctor. But
after observing experienced doctors treating their patients with pills
and procedures, he realized that these authoritative doctors didn't do
any better than he did. Their patients didn't just stay sick — they got
worse. John realized something was wrong with the system, not him,
so he began to read the scientific literature. Like Dr. Esselstyn, once
he started reading the literature, John became convinced that a whole
foods, plant-based diet had the potential not only to prevent these dis-
eases that were plaguing patients, but also the potential to treat them.
This idea, he was to find out, was not received kindly by his teachers
and colleagues.

In this environment, diet was considered quackery. John would ask,
"Doesn't diet have something to do with heart disease?" and his col-
leagues would tell him that the science was controversial. John contin-
ued to read the scientific research and to talk to his colleagues and only
became even more baffled. "When I looked at the literature, I couldn't
find the controversy. It was absolutely clear what the literature said."
Through those years, John came to understand why so many physicians
claimed diet was controversial: "The scientist is sitting down at the
breakfast table and in the one hand he has a paper that says that cho-
lesterol will rot your arteries and kill you, and in the other hand he has
a fork shoveling bacon and eggs into his mouth, and he says, 'There's

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331

something confusing here. I'm confused.' And that's the controversy.
That's all it is."

John tells a story about seeing a thirty-eight-year-old man and his
wife after the man had suffered a second heart attack. As the attending
resident (not their primary physician), he asked the patient what he
was going to do to prevent a third, fatal heart attack. "You're thirty-eight
years old with a beautiful young wife, five kids. What are you going to
do to keep your wife from being a widow and your kids from becom-
ing fatherless?" The man was despondent, frustrated and said, "There's
nothing I can do. I don't drink. I don't smoke. I exercise, I follow the
same diet the dietitian gave me after my last heart attack. There's noth-
ing more I can do."

John told the couple what he had been learning about diet. He sug-
gested that the man might reverse his disease if he ate the right way. The
patient and his wife received the news with enthusiasm. John talked
with them for quite a long time, left the room and felt great. He had
finally helped someone; he had finally done his job.

That lasted for about two hours. He was called into the Chief of Med-
icine's office. The Chief of Medicine wields absolute authority over the
residents. If he fires a resident, not only is that person out of his or her
job, that person is out of his or her career. The excited couple had told
their primary physician what they had just learned. The doctor replied
that what they had been told wasn't true, and promptly reported John to
the Chief of Medicine.

The Chief of Medicine had a serious conversation with John, who
remembers being told that "I was stepping far beyond my duties as
a resident. I should get serious about medicine and give up all this
nonsense about food having anything to do with disease." The Chief
of Medicine made it clear that on this point, John's job, and his sub-
sequent career, was on the line. So John bit his tongue for the rest of
his education.

On the day of John's graduation, he and the Chief of Medicine had a
final talk. John remembers the man as being smart, with a good heart,
but he was too entrenched in the status quo. The Chief of Medicine sat
him down and said, "John, I think you're a good doctor. I want you to
know that. I want you to know that I like your family. That's why I'm
going to tell you this. I'm concerned that you're going to starve to death
with all your crazy ideas about food. All you're going to do is collect a
bunch of bums and hippies."

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John paused to gather his thoughts, and then said, "That may be the
case. Then I'll have to starve. I can't put people on drugs or surgeries
that don't work. Besides, I think you're wrong. I don't think it will be
bums and hippies. I think it will be successful people who have done
well in life. They'll ask themselves, 'I'm such a big success, so how come
I'm so fat?'" With that, John looked at the Chief's generous belly, and
continued, "They'll ask, 'If I'm such a big success, why are my health
and my future out of control?' They'll look at what I have to say, and
they're going to buy it."

John finished his formal medical education having had only one hour
of nutrition instruction, which involved learning which infant formulas
to use. His experience confirms every study that has found nutrition
training among physicians to be sorely inadequate.

HOOKED ON DRUGS

John touched on another important area where the medical profession
has lost credibility: its ties with the drug industry. Medical education
and drug companies are in bed together, and have been for quite some
time. John talked some about the depth of the problem and how the
educational system has been corrupted. He said:

The problem with doctors starts with our education. The whole
system is paid for by the drug industry, from education to research.
The drug industry has bought the minds of the medical profession.
It starts the day you enter medical school. All the way through
medical school everything is supported by the drug industry.

John is not alone in criticizing the way in which the medical estab-
lishment has partnered with the drug industry. Many prominent sci-
entists have published scathing observations showing how corrupt the
system has become. Among the common observations are:

• The drug industry ingratiates itself with medical students with
free gifts, including meals, entertainment and travel; educational
events, including lectures, which are little more than drug adver-
tisements; and conferences, which include speakers who are little
more than drug spokespeople. 15-17

• Graduate medical students (physician residents) and other physi-
cians actually change their prescribing habits because of informa-
tion provided by drug salespeople, 18-20 even though this information

BIG MEDICINE: WHOSE HEALTH ARE THEY PROTECTING?

333

is known to be "overly positive and prescribing habits are less ap-
propriate as a result." 17 ' 21,22

• Research and academic medicine merely carry out the pharmaceu-
tical industry's bidding. This can happen because: the drug com-
panies, and not researchers, may design the research, which allows
the company to "rig" the study 23, 24 ; the researchers may have a
direct financial stake in the drug company whose product they are
studying 15, 25 ; the drug company may be responsible for collecting
and collating the raw data, and then only selectively allowing re-
searchers to view the data 23, 26 ; the drug company may retain veto
power over whether the findings are published, and may retain
editorial rights over any scientific publications resulting from the
research 23 - 25,27 ; the drug company may hire a communications firm
to write the scientific article, and then find researchers willing to
attach their names as authors of the paper after it has already been
written. 26

• The major scientific journals have turned into little more than mar-
keting vehicles for drug companies. The leading medical journals
derive their primary income from drug advertising. This advertis-
ing is not adequately reviewed by the journal, and companies often
present misleading claims about drugs. Perhaps more disconcert-
ing, the majority of clinical trial research reported in the journals is
funded by drug company money, and the financial interests of the
researchers involved are not fully acknowledged. 24

In the past couple of years there have been well-publicized scandals
at major medical centers that confirm these charges. In one instance,
a scientist's integrity was maligned in a variety of ways by both a drug
company and her university administration after she found that a drug
under study had strong side effects and it lost its effectiveness. 27 In an-
other case, a scientist speaking out about the possible side effects of
antidepressants lost a job opportunity at the University of Toronto. 26
The examples go on and on.

Dr. Marcia Angell, an ex-editor of the New England Journal of Medicine,
wrote a scathing editorial called "Is Academic Medicine for Sale?" 15 :

The ties between clinical researchers and industry include not
only grant support, but also a host of other financial arrangements.
Researchers serve as consultants to companies whose products
they are studying, join advisory boards and speakers' bureaus,

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enter into patent and royalty arrangements, agree to be the listed
authors of articles ghostwritten by interested companies, promote
drugs and devices at company-sponsored symposiums and allow
themselves to be plied with expensive gifts and trips to luxurious
settings. Many also have equity interest in the companies.

Dr. Angell goes on to say that these financial associations often sig-
nificantly "bias research, both the kind of work that is done and the way
it is reported."

Even more dangerous than the threat of fraudulent findings is the
fact that the only type of research that is funded and recognized is
research on drugs. Research on the causes of disease and non-drug
interventions simply doesn't occur in medical education settings. For
example, academic researchers may be furiously trying to find a pill
that will treat the symptoms of obesity, but not be devoting any time
or money to teaching people how to live a healthier life. Dr. Angell
writes 15 :

In terms of education, medical students and house officers, under
the constant tutelage of industry representatives, learn to rely on
drugs and devices more than they probably should [my emphasis].
As the critics of medicine so often charge, young physicians learn
that for every problem, there is a pill [my emphasis] (and a drug
company representative to explain it). They also become accus-
tomed to receiving gifts and favors from an industry that uses
these courtesies to influence their continuing education. The aca-
demic medical centers, in allowing themselves to become research
outposts for industry, contribute to the overemphasis on drugs and
devices."

In this environment, is it possible for nutrition to be given fair and
honest consideration? Despite the fact that our leading killers can be
prevented and even reversed using good nutrition, will you ever hear
about it from your doctor? Not as long as this environment persists in
our medical schools and hospitals. Not unless your doctor has decided
that standard medical practice as it is taught does not work, and decides
to spend a significant amount of time educating himself or herself about
good nutrition. This takes a rare individual.

The situation has gotten so bad that Dr. John McDougall said, "I
don't know what to believe anymore. When I read a paper that says I

BIG MEDICINE: WHOSE HEALTH ARE THEY PROTECTING?

335

should be giving my heart patients beta blockers and ACE inhibitors,
two classes of heart drugs, I don't know whether it's true. I honestly don't
know if it's true because [drug research] is so tainted."
Do you think the following headlines are related?

"Schools report research interest conflicts" (between drug companies

and researchers) 28
"Prescription use by children multiplying, study says" 29
"Survey: Many guidelines written by doctors with ties to companies" 30
"Correctly Prescribed Drugs Take Heavy Toll; Millions Affected by

Toxic Reactions" 31

We pay a high price for allowing these medical biases. A recent study
found that one in five new drugs will either get a "black box warning,"
indicating a previously unknown serious adverse reaction that may re-
sult in death or serious injury, or will be withdrawn from the market
within twenty-five years. 32 Twenty percent of all new drugs have serious
unknown side effects, and more than 100,000 Americans die every year
from correctly taking their properly prescribed medication. 33 This is one
of the leading causes of death in America!

DR. MCDOUGALL'S FATE

When Dr. John McDougall finished his formal medical education, he set
up a practice on the Hawaiian island of Oahu. He began writing books
about nutrition and health and established a national reputation. In the
mid-1980s John was contacted by St. Helena Hospital in Napa Valley,
California, and asked if he would accept a position running its health
center. The hospital was a Seventh-day Adventist hospital; if you recall
from chapter seven, the Seventh-day Adventists encourage followers to
eat a vegetarian diet (even though they consume higher-than-average
amounts of dairy products). It was an opportunity too good to pass up,
and John left Hawaii and headed for California.

John had a good home at St. Helena for a number of years. He taught
nutrition and used nutrition to treat sick patients, which he did with
fantastic success. He treated over 2,000 very sick patients, and over the
course of sixteen years, he has never been sued or even had a letter of
complaint. Perhaps more importantly, John saw these patients get well.
Throughout this time, he continued his publishing activity, maintaining
a national reputation. But as time passed, he realized that things weren't
quite the same as when he first arrived. His discontent was growing.

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Of those later years he says, "I just didn't think I was going anyplace.
The program had 150 or 170 people a year and that was it. Never grew.
Wasn't getting any support from the hospital and we had gone through
a lot of administrators."

He had small clashes with the other doctors at the hospital. At one
point, the heart department objected to what John was doing with heart
patients. John told them, "I'll tell you what, I'll send every one of my
heart patients to you for a second opinion if you'll send yours to me." It
was quite an offer, but they didn't accept it. On another occasion John
had referred a patient to a cardiologist and the cardiologist incorrectly
told the patient that he needed to have bypass surgery. After a couple
of these incidents, John had reached the limit of his patience. Finally
after the cardiologist recommended surgery for another one of John's
patients, John called him and said, "I want to talk with you and the
patient about this. I would like to discuss the scientific literature that
causes you to make this recommendation." The cardiologist said that he
wouldn't do that, to which John responded, "Why not? You just recom-
mended that this guy have his heart opened! And you're going to charge
him 50,000 or 100,000 bucks for it. Why don't we discuss it? Don't you
think that's fair to the patient?" The cardiologist declined, saying that it
would just confuse the patient. That was the last time he recommended
heart surgery for one of John's patients.

Meanwhile, none of the other physicians in the hospital had ever
referred a patient to John. Not once. Other physicians would send their
own wives and children to see him but they would never refer a patient.
The reason, according to John:

They were worried [about what would happen when] their pa-
tients would come to see me, and it happened all the time when
patients would come on their own. They'd come to me with heart
disease or high blood pressure or diabetes. I'd put them on the diet
and they'd go back off all their pills and soon their numbers would
be normal. They'd go to their doctor and say, "Why the hell didn't
you tell me about this before? Why did you let me suffer, spend all
this money, almost die, when all I had to do was eat oatmeal?" The
doctors didn't want to hear this.

There were other moments of friction between John and the hospital,
but the last straw involved the Dr. Roy Swank multiple sclerosis pro-
gram mentioned in chapter nine.

BIG MEDICINE: WHOSE HEALTH ARE THEY PROTECTING?

337

John had contacted Dr. Swank when he learned that Swank was
about to retire. John had known and respected Dr. Roy Swank for a long
time, and he offered to take over the Swank multiple sclerosis program
and merge it with his health clinic at St. Helena Hospital, preserving it
in honor of Dr. Swank. Dr. Swank agreed, much to John's excitement.
As John said, there were four reasons that this would be a perfect fit for
St. Helena's:

• it fit in with the philosophy of the Adventists: dietary treatment of
disease

• they would be helping people who desperately needed their help

• it would double their patient census, helping to grow the pro-
gram

• it would cost almost nothing

In thinking back on it, John said, "Could you think of any reason not
to do this? It [was] obvious!" So he took the proposal to the head of his
department. After listening, she said that she didn't think the hospital
wanted to do this. She said, "Well, I don't think we really want to in-
troduce any new programs right now." John, dumbfounded, asked her,
"Please tell me why. What does it mean to be a hospital? Why are we
here? I thought we were here to take care of sick people."

Her response was a doozy: "Well, you know we are, but you know,
MS patients are not really desirable patients. You told me yourself that
most neurologists don't like to take care of MS patients." John could not
believe what he had just heard. In a very tense moment, he said:

Wait a minute. I'm a doctor. This is a hospital. As far as 1 know our
job is to relieve the suffering of the sick. These are sick people. Just
because other doctors can't help them in their suffering doesn't
mean that we can't. Here's the evidence that says we can. I have
an effective treatment for people who need my care and this is a
hospital. Will you explain to me why we don't want to take care of
those kinds of patients?

He continued:

I want to talk to the head of the hospital. I want to explain to her
why I need this program and why the hospital needs this program
and why the patients need this program. I want you to get me an
appointment.

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Ultimately, though, the head of the hospital proved to be just as dif-
ficult. John reflected on the situation with his wife. He was supposed to
renew his contract with the hospital in a couple of weeks, and he decid-
ed not to do it. He left on cordial terms, and to this day he does not hold
personal grudges. He just explains it by saying that their directions in
life were different. John would prefer to remember St. Helena for what it
was: a good home to him for sixteen years, but a place nonetheless that
was "just into that whole drug money thing."

Now, John runs a highly successful "lifestyle medicine" program with
his family's help, writes a popular newsletter that he makes freely avail-
able (http://www.drmcdougall.com), organizes group trips with past
patients and new friends and has more time to go windsurfing when the
wind picks up on Bodega Bay. This is a man with a wealth of knowledge
and qualifications, who could benefit the health of millions of Ameri-
cans. He has never been challenged by any of his colleagues for physi-
cian "misbehavior," and yet the medical establishment does not want
his services. He is reminded of this fact all the time:

Patients will come in with rheumatoid arthritis. They'll be in
wheelchairs, they can't even turn the key on their car. And I'll
take care of them and three or four weeks later, they'll go back to
see their doctor. They'll walk up to their doctor, grab their hand
and shake it hard. Doctor will say, "Wonderful." The patient, all
excited, will say, "Well, I want to tell you what I did. I went to
see this Dr. McDougall, I changed my diet, and now my arthritis
is gone." Their doctor simply responds, "Oh my goodness. That's
great. Whatever you're doing, just keep doing it. I'll see you later."
That's always the response. It's not, "Please, my god, tell me what
you did so I can tell the next patient." It's, "Whatever you're doing,
that's just great." If the patient starts to tell them they changed to a
vegetarian diet, the doctor will cut in with, "Yeah okay, fine, you're
really a strong person. Thanks a lot. See you later." Get them out
of the office as quickly as they can. It's very threatening ... very
threatening.

ESSELSTYN'S REWARD

Back in Ohio, Dr. Esselstyn retired from active surgery in June of 2000
and assumed the position of preventive cardiology consultant in the de-
partment of general surgery at the Cleveland Clinic. He has continued

BIG MEDICINE: WHOSE HEALTH ARE THEY PROTECTING? 339

to do research and to visit with patients. He holds three-hour counsel-
ing sessions in his home with new heart disease patients, gives them re-
search evidence and provides a delicious "heart-safe" meal. In addition,
he gives talks around the country and abroad.

In March of 2002, Ess and his wife Ann, whose grandfather founded
the Cleveland Clinic, drafted a letter to the head of the cardiology de-
partment and the head of the hospital at the Cleveland Clinic. The letter
started off by saying how proud they were of the reputation and excel-
lence of the Clinic and the innovation of the surgical procedures, but
that everyone recognized that surgery was never going to be the answer
to this epidemic of heart disease. Ess formally proposed the idea that he
could help set up an arrest and reversal dietary program in the depart-
ment of preventive cardiology at the Cleveland Clinic. The program
would mirror his own and could be administered by nurse clinicians
and physician assistants. Ideally a young physician with passion for
the idea would head the program. Ultimately, every patient with heart
disease at the Clinic would be offered the option of arrest and reversal
therapy using dietary means, which costs very little, harbors no risks
and puts the control back into the patients' hands.

You'd think that if an opportunity arose to profoundly heal sick
people, and one of the most reputable people in the country was going
to help you, a hospital would jump at the opportunity. But after being
one of the star surgeons at the Cleveland Clinic for decades, after initi-
ating a heart reversal study that had greater success than anything ever
done at the Clinic, and after graciously offering a plan to help heal even
more people, neither the head of the hospital nor the department head
had the respect to even acknowledge that Ess had written to them. They
didn't call. They didn't write. They completely ignored him.

Seven weeks passed, and finally Ess called the department head and
the hospital head, and neither of them would take his call. Finally, after
seven calls, the head of the hospital got on the phone. This man had
praised Ess for years for his research and seemed excited by his results,
but now he was singing a different tune. He obviously knew exactly
what Ess was calling about, and told Ess that the head of the cardiol-
ogy department didn't want to do it. In other words, he just passed the
buck. If the head of the hospital wanted it to be done, it would be done,
regardless of what the head of cardiology wanted. So Ess called the head
of cardiology, who finally took his call. The man was abrasive and rude.
He made it clear he had no interest in what Ess was trying to do.

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THE CHINA STUDY

Ess hasn't talked to either of these doctors since, but he still has hope
that he can change their minds as more and more research supports
what he has been saying. Meanwhile, many people at the Clinic are still
excited about Ess's work. Many of them want to see a wider application
of his program, but the powers that be will not let it happen. They get
frustrated, and Ess is frustrated because the current program in preven-
tive cardiology is a disaster:

They still eat meat, they still eat dairy, and they don't have any
cholesterol goal. It's all just so vague. Preventive cardiology takes
great pride when they are able to slow the rate of progression of
this disease. This isn't cancer for God's sake!

An interesting situation is now developing: just as with Dr. McDou-
gall, many of the Clinic "bigwigs" with heart disease have themselves
gone to Esselstyn for treatment and lifestyle counseling. They know it
works, and they seek out the program on their own. As Ess says, this
could be developing into a very interesting crisis:

I have now treated a number of senior staff with coronary disease
at the Clinic — senior staff physicians. I have also treated a number
of senior staff trustees. One of the trustees knows about the frustra-
tions that we've had trying to get this into the Clinic, and he says,
"I think, if the word gets out that Esselstyn has this treatment that
arrests and reverses this disease at the Cleveland Clinic, and it's been
used by senior staff and he's treated senior trustees, but he's not per-
mitted to treat the common herd, we could be open for a lawsuit."

For the time being, Ess, with his wife's help, will continue to run
counseling sessions out of his own home because the institution to
which he gave the greater part of his life does not want to endorse a
dietary approach that competes with its standard menu of pills and
procedures. This past summer Ess spent much more time than usual
at his upstate New York farm, making hay. As much as Ess likes a more
relaxed life, he would also love to continue to help diseased people get
better with the aid of the Cleveland Clinic. But they won't allow him
to. As far as I am concerned, this is nothing short of criminal. We, the
public, turn to doctors and hospitals in times of great need. For them
to provide care that is knowingly less than optimal, that doesn't protect
our health, doesn't heal our disease and costs us tens of thousands of
dollars is morally inexcusable. Ess sums up the situation:

BIG MEDICINE: WHOSE HEALTH ARE THEY PROTECTING?

341

The Clinic is now injecting stem cells to try to make new heart
vessels grow. Wouldn't it be easier to stop the disease? It's appall-
ing, isn't it? It's just so grippingly unbelievable to think that we're
being led around by people who refuse to believe the obvious!

Both Esselstyn and McDougall have now been denied reentry into
the establishment, after headline-making success at healing people with
a nutritional approach. You can focus on the money — according to John
and Ess, 80% of St. Helena's and 65% of the Cleveland Clinic's respective
incomes were generated by traditional heart disease treatments, surgi-
cal interventions — but it's something more than just money. It may also
be the intellectual threat that the patient should be in control, and not
the doctor; that something as simple as food could be more powerful
than all the knowledge of pills and high-tech procedures; it may be the
lack of credible nutrition education in medical school; it may be the
influence of the drug industry. Whatever it is, it has become clear that
the medical industry in this country is not protecting our health as it
should. As McDougall reaches his arms out, palms up, and scrunches
his shoulders up, he simply says, "It's beyond comprehension."

Repeating Histories

In 1985, when I was on sabbatical in Oxford, England, I had the op-
portunity to study the history of diet and disease at some of the great
medical history libraries in the Western world. I made use of the famous
Bodlean Library in Oxford and the London libraries of the Royal Col-
lege of Surgeons and the Imperial Cancer Research Fund. In the quiet
recesses of these marble-lined sanctuaries, I was thrilled to find authors
who wrote eloquently on the topic of diet and cancer, among other dis-
eases, over 150 years ago.

One such author was George Macilwain, who wrote fourteen books
on medicine and health. Macilwain was born and raised in Northern
Ireland. He later moved to London where he became a prominent sur-
geon in the early 1800s. He was to become a member, and later, an hon-
orary fellow, of the Royal College of Surgeons. He became vegetarian at
the age of forty, after identifying "grease, fat and alcohol" as being the
chief causes of cancer. 1 Macilwain also popularized the theory of the
"constitutional nature of disease," mostly in reference to the origins and
treatment of cancer.

The constitutional nature of disease concept meant that disease is not
the result of one organ, one cell or one reaction gone awry or the result
of one external cause acting independently. It is the result of multiple
systems throughout the body breaking down. Opposing this view was the
local theory of disease, which said that disease is caused by a single
external agent acting at a specific site in the body At that time, a fierce
fight was under way between those who believed in diet and those who

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supported surgery and the emerging use of drugs. The "local disease"
proponents argued that disease was locally caused and could be cut
out or locally treated with isolated chemicals. In contrast, those who
favored diet and lifestyle believed that disease was a symptom resulting
from the "constitutional" characteristics of the whole body.

I was impressed that these old books contained the same ideas about
diet and disease that had resurfaced in the health battles of the 1980s. As
I learned more about Macilwain, I came to realize that he was a relative
of mine. My paternal grandmother's maiden name was Macilwain, and
that "branch" of the family had lived in the same part of Northern Ireland
that George Macilwain had come from. Furthermore, there were family
stories about a famous Macilwain who had left the family farm in Ireland
to become a very well-known doctor in London in the early 1800s. My fa-
ther, who had emigrated from Northern Ireland, had referred to an Uncle
George when I was young, but I never was aware of who this man was.
Through further genealogical research, I have come to the near certain
conclusion that George Macilwain was my great-great uncle.

This discovery has been one of the more remarkable stories of my

life. My wife Karen says, "If there's such a thing as reincarnation "

I agree: if I ever lived a past life, it was as George Macilwain. He and I
had similar careers; both of us became acutely aware of the importance
of diet in disease, and both of us became vegetarian. Some of his ideas,
written over 150 years ago, were so close to what I believed that I felt
they could have come from my own mouth.

I discovered more than my family history while reading in these au-
gust, history-laden libraries. I found out that scholars have been arguing
over the nature of health for centuries, even millennia. Almost 2,500
years ago, Plato wrote a dialogue between two characters, Socrates and
Glaucon, in which they discuss the future of their cities. Socrates says
the cities should be simple, and the citizens should subsist on barley
and wheat, with "relishes" of salt, olives, cheese and "country fare of
boiled onions and cabbage," with desserts of "figs, pease, beans," roasted
myrtle-berries and beechnuts, and wine in moderation. 2 Socrates says,
"And thus, passing their days in tranquility and sound health, they will,
in all probability, live to an advanced age "

But Glaucon replies that such a diet would only be appropriate for "a
community of swine," and that the citizens should live "in a civilized
manner." He continues, "They ought to recline on couches . . . and have
the usual dishes and dessert of a modern dinner." In other words, the

REPEATING HISTORIES

345

citizens should have the "luxury" of eating meat. Socrates replies, "if
you wish us also to contemplate a city that is suffering from inflam-
mation We shall also need great quantities of all kinds of cattle for

those who may wish to eat them, shall we not?"

Glaucon says, "Of course we shall." Socrates then says, "Then shall
we not experience the need of medical men also to a much greater ex-
tent under this than under the former regime?" Glaucon can't deny it.
"Yes, indeed," he says. Socrates goes on to say that this luxurious city
will be short of land because of the extra acreage required to raise ani-
mals for food. This shortage will lead the citizens to take land from oth-
ers, which could precipitate violence and war, thus a need for justice.
Furthermore, Socrates writes, "when dissoluteness and diseases abound
in a city, are not law courts and surgeries opened in abundance, and do
not Law and Physic begin to hold their heads high, when numbers even
of well-born persons devote themselves with eagerness to these profes-
sions?" In other words, in this luxurious city of sickness and disease,
lawyers and doctors will become the norm. 2

Plato, in this passage, made it perfectly clear: we shall eat animals
only at our own peril. Though it is indeed remarkable that one of the
greatest intellectuals in the history of the Western world condemned
meat eating almost 2,500 years ago, I find it even more remarkable that
few know about this history. Hardly anybody knows, for example, that
the father of Western medicine, Hippocrates, advocated diet as the chief
way to prevent and treat disease or that George Macilwain knew that
diet was the way to prevent and treat disease or that the man instru-
mental in founding the American Cancer Society, Frederick L. Hoffman,
knew that diet was the way to prevent and treat disease.

How did Plato predict the future so accurately? He knew that con-
suming animal foods would not lead to true health and prosperity. In-
stead, the false sense of rich luxury granted by being able to eat animals
would only lead to a culture of sickness, disease, land disputes, lawyers
and doctors. This is a pretty good description of some of the challenges
faced by modern America!

How did Seneca, one of the great scholars 2,000 years ago, a tutor
and advisor to Roman Emperor Nero, know with such certainty the
trouble with consuming animals when he wrote 2 :

An Ox is satisfied with the pasture of an acre or two: one wood
suffices for several Elephants. Man alone supports himself by the

346 THE CHINA STUDY

pillage of the whole earth and sea. What! Has Nature indeed given
us so insatiable a stomach, while she has given us so insignificant
bodies? . . . The slaves of the belly (as says Sallust) are to be count-
ed in the number of the lower animals, not of men. Nay, not of

them, but rather of the dead You might inscribe on their doors,

"These have anticipated death."

How did George Macilwain predict the future when he said that the
local theory of disease would not lead to health? Even today, we don't
have any pills or procedures that effectively prevent, eliminate or even
treat the causes of any chronic diseases. The most promising preven-
tions and treatments have now been shown to be diet and lifestyle
changes, a constitutional approach to health.

How did we forget these lessons from the past? How did we go from
knowing that the best athletes in the ancient Greek Olympics must
consume a plant-based diet to fearing that vegetarians don't get enough
protein? How did we get to a place where the healers of our society, our
doctors, know little, if anything, about nutrition; where our medical
institutions denigrate the subject; where using prescription drugs and
going to hospitals is the third leading cause of death? How did we get
to a place where advocating a plant-based diet can jeopardize a profes-
sional career, where scientists spend more time mastering nature than
respecting it? How did we get to a place where the companies that profit
from our sickness are the ones telling us how to be healthy; where the
companies that profit from our food choices are the ones telling us
what to eat; where the public's hard-earned money is being spent by
the government to boost the drug industry's profits; and where there is
more distrust than trust of our government's policies on foods, drugs
and health? How did we get to a place where Americans are so confused
about what is healthy that they no longer care?

Our country's population, which numbers almost 300 million peo-
ple, 3 is sick.

• 82% of American adults have at least one risk factor for heart dis-
ease 1

• 81% of Americans take at least one medication during any given
week 5

• 50% of Americans take at least one prescription drug during any
given week 5

• 65% of American adults are overweight 6

REPEATING HISTORIES

347

• 31% of American adults are obese 6

• Roughly one in three youths in America (ages six to nineteen) is
already overweight or at risk of becoming overweight

• About 105 million American adults have dangerously high choles-
terol levels 7 (denned as 200 mg/dL or higher — heart-safe choles-
terol level is under 150 mg/dL)

• About 50 million Americans have high blood pressure 8

• Over 63 million American adults have pain in the lower back
(considerably related to circulation and excess body weight, both
influenced by diet and aggravated by physical inactivity) during
any given three-month period 9

• Over 33 million American adults have a migraine or severe head-
ache during any given three-month period 9

• 23 million Americans had heart disease in 200 1 9

• At least 16 million Americans have diabetes

• Over 700,000 Americans died from heart disease in 2000

• Over 550,000 Americans died from cancer in 2000

• Over 280,000 Americans died from cerebro-vascular diseases
(stroke), diabetes or Alzheimer's in 2000

At the great peril of ignoring the warnings of Plato and others, Amer-
ica has, in the words of Seneca, "anticipated death." Starvation, poor
sanitation and communicable diseases, symbols of impoverishment,
have been largely minimized in the Western world. Now we have an
urgency of excess, and some of the previously less developed countries
are racing to get where we are. Never before have such large percentages
of the population died from diseases of "affluence." Is this the affluence
that Socrates predicted 2,500 years ago — a society full of doctors and
lawyers wrestling with the problems caused by people living luxuri-
ously and eating cattle? Never before have so many people suffered such
high levels of obesity and diabetes. Never before has the financial strain
of health care distressed every sector of our society, from business to
education to government to everyday families with inadequate insur-
ance. If we have to decide between health insurance for our teachers
and textbooks for our kids, which will we choose?

Never before have we affected the natural environment to such an ex-
tent that we are losing our topsoil, our massive North American aquifers,
and our world's rainforests. 10 We are changing our climate so rapidly that
many of the world's best-informed scientists fear the future. Never before

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THE CHINA STUDY

have we been eliminating plant and animal species from the face of the
earth as we are doing now. Never before have we introduced, on such a
large scale, genetically altered varieties of plants into the environment
without knowing what the repercussions will be. All of these changes in
our environment are strongly affected by what we choose to eat. 11

As the billions of people in the developing world are accumulating
more wealth and adopting the Western diet and lifestyle, problems cre-
ated by nutritional excess are becoming exponentially more urgent with
each passing year. In 1997, the director-general of the World Health Orga-
nization, Dr. Hiroshi Nakajima, referred to the future chronic disease bur-
den in developing countries as "a crisis of suffering on a global scale." 12

We've fumbled around for the past 2,500 years, building up the un-
sustainable behemoth that we now call modern society. We certainly
won't have another 2,500 years to remember the teachings of Plato,
Pythagoras, Seneca and Macilwain; we won't even have 250 years. From
this urgency arises great opportunity, and because of that I am filled
with hope. People are beginning to sense the need for change and are
beginning to question some of the most basic assumptions that we have
about food and health. People are beginning to understand the conclu-
sions of scientific literature and are changing their lives for the better.

Never before has there been such a mountain of empirical research
supporting a whole foods, plant-based diet. Now, for example, we can
obtain images of the arteries in the heart, and then show conclusively,
as Drs. Dean Ornish and Caldwell Esselstyn, Jr., have done, that a whole
foods, plant-based diet reverses heart disease. 13 We now have the knowl-
edge to understand how this actually works. Animal protein, even more
than saturated fat and dietary cholesterol, raises blood cholesterol levels
in experimental animals, individual humans and entire populations.
International comparisons between countries show that populations
subsisting on traditional plant-based diets have far less heart disease, and
studies of individuals within single populations show that those who eat
more whole, plant-based foods not only have lower cholesterol levels, but
have less heart disease. We now have a deep and broad range of evidence
showing that a whole foods, plant-based diet is best for the heart.

Never before have we had such a depth of understanding of how diet
affects cancer both on a cellular level as well as a population level. Pub-
lished data show that animal protein promotes the growth of tumors.
Animal protein increases the levels of a hormone, IGF-1, which is a risk
factor for cancer, and high-casein (the main protein of cow's milk) diets
allow more carcinogens into cells, which allow more dangerous carcino-

REPEATING HISTORIES

349

gen products to bind to DNA, which allow more mutagenic reactions
that give rise to cancer cells, which allow more rapid growth of tumors
once they are initially formed. Data show that a diet based on animal-
based foods increases a female's production of reproductive hormones
over her lifetime, which may lead to breast cancer. We now have a deep
and broad range of evidence showing that a whole foods, plant-based diet is
best for cancer.

Never before have we had technology to measure the biomarkers
associated with diabetes, and the evidence to show that blood sugar,
blood cholesterol and insulin levels improve more with a whole foods,
plant-based diet than with any other treatment. Intervention studies
show that Type 2 diabetics treated with a whole foods, plant-based diet
may reverse their disease and go off their medications. A broad range of
international studies shows that Type 1 diabetes, a serious autoimmune
disease, is related to cow's milk consumption and premature weaning.
We now know how our autoimmune system can attack our own bod-
ies through a process of molecular mimicry induced by animal proteins
that find their way into our bloodstream. We also have tantalizing
evidence linking multiple sclerosis with animal food consumption, and
especially dairy consumption. Dietary intervention studies have shown
that diet can help slow, and perhaps even halt, multiple sclerosis. We
now have a deep and broad range of evidence showing that a whole foods,
plant-based diet is best for diabetes and autoimmune diseases.

Never before have we had such a broad range of evidence showing that
diets containing excess animal protein can destroy our kidneys. Kidney
stones arise because the consumption of animal protein creates excessive
calcium and oxalate in the kidney. We know now that cataracts and age-
related macular degeneration can be prevented by foods containing large
amounts of antioxidants. In addition, research has shown that cognitive
dysfunction, vascular dementia caused by small strokes and Alzheimer's
are all related to the food we eat. Investigations of human populations
show that our risk of hip fracture and osteoporosis is made worse by di-
ets high in animal-based foods. Animal protein leeches calcium from the
bones by creating an acidic environment in the blood. We now have a deep
and broad range of evidence showing that a whole foods, plant-based diet is
best for our kidneys, bones, eyes and brains.

More research can and should be done, but the idea that whole foods,
plant-based diets can protect against and even treat a wide variety of
chronic diseases can no longer be denied. No longer are there just a few
people making claims about a plant-based diet based on their personal

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THE CHINA STUDY

experience, philosophy or the occasional supporting scientific study.
Now there are hundreds of detailed, comprehensive, well-done research
studies that point in the same direction.

Furthermore, I have hope for the future because of our new abil-
ity to exchange information across the country and around the world.
A much greater proportion of the world population is literate, and a
much greater proportion of that population has the luxury of choosing
what they eat from a wide variety of readily accessible foods. People can
make a whole foods, plant-based diet varied, interesting, tasty and con-
venient. I have hope because people in small towns and in previously
isolated parts of the country can now readily access cutting edge health
information and put it into practice.

All of these things together create an atmosphere unlike any other,
an atmosphere that demands change. Contrary to the situation in 1982,
when a few colleagues tried to destroy the reputations of scientists who
suggested that diet had anything to do with cancer, it is now more com-
monly accepted that what you eat can determine your risk of multiple
cancers. I have also seen the public image of vegetarianism emerge from
being considered a dangerous, passing fad to a healthful, enduring life-
style choice. The popularity of plant-based diets has been increasing,
and both the variety and availability of convenient vegetarian foods have
been skyrocketing. 14 Restaurants around the country now regularly offer
meat-free and dairy-free options. 15 Scientists are publishing more articles
about vegetarianism and writing more about the health potential of a
plant-based diet. 16 Now, over 150 years after my great-great uncle George
Macilwain wrote books about diet and disease, I am writing a book about
diet and disease with the help of my youngest son Tom. Tom's middle
name is Mcllwain (the family changed the spelling over the past couple
of generations), which means that not only am I writing about many of
the same ideas Macilwain wrote about, but a relative bearing his name is
the co-author. History can repeat itself. This time, however, instead of the
message being forgotten and confined to library stacks, I believe that the
world is finally ready to accept it. More than that, I believe the world is
finally ready to change. We have reached a point in our history where our
bad habits can no longer be tolerated. We, as a society, are on the edge of
a great precipice: we can fall to sickness, poverty and degradation, or we
can embrace health, longevity and bounty. And all it takes is the courage
to change. How will our grandchildren find themselves in 100 years?
Only time will tell, but I hope that the history we are witnessing and the
future that lies ahead will be to the benefit of us all.

APPENDIX A

Q&A: Protein Effect in
Experimental Rat Studies

COULD THE DIETARY PROTEIN EFFECT
BE DUE TO OTHER NUTRIENTS IN THE RAT DIET?

Decreasing dietary protein from 20% to 5% means finding something to
replace the missing 15%. We used a carbohydrate to replace the casein
because it had the same energy content. As dietary protein decreased,
a 1:1 mixture of starch and glucose increased by the same amount.
The extra starch and glucose in the low-protein diets could not have
been responsible for the lower development of foci because these car-
bohydrates, when tested alone, actually increase foci development. 1 If
anything, a little extra carbohydrate in the low-protein diet would only
increase cancer incidence and offset the low-protein effect. This makes
prevention of cancer by low-protein diets even more impressive.

MIGHT THE PROTEIN EFFECT BE DUE
TO THE RATS ON A LOW-PROTEIN DIET
EATING LESS FOOD (I.E., LESS CALORIES)?

Many studies done in the 1930s, 1940s and 1950s 2 had shown that
decreasing total food intake, or total calories, decreased tumor devel-
opment. A review of our many experiments, however, showed that
animals fed the low-protein diets did not consume less calories but, on

351

352

THE CHINA STUDY

average, actually consumed more calories. 3 - 4 Again, this only reinforced
the tumor-promoting effect observed for casein.

WHAT WAS THE OVERALL HEALTH OF THE RATS
ON A LOW-PROTEIN DIET?

Many researchers have long assumed that animals fed diets this low in
protein would not be healthy However, the low-protein animals were
healthier by every indication. They lived longer, were more physically
active, were slimmer and had healthy hair coats at 100 weeks while the
high-protein counterpart rats were all dead. Also, animals consuming
less dietary casein not only ate more calories, but they also burned off
more calories. Low-protein animals consumed more oxygen, which is
required for the burning of these calories, and had higher levels of a spe-
cial tissue called brown adipose tissue, 5 6 which is especially effective in
burning off calories. This occurs through a process of "thermogenesis,"
i.e., the expenditure of calories as body heat. This phenomenon had
already been demonstrated many years before. 7-11 Low-protein diets en-
hance the burning off of calories, thus leaving less calories for body weight
gain and perhaps also less for tumor growth as well.

WAS PHYSICAL ACTIVITY RELATED TO THE
CONSUMPTION OF THE LOW-PROTEIN DIET?

To measure the physical activity of each group of rats, we compared
how much they voluntarily operated an exercise wheel attached to their
cages. A monitor recorded the number of times the animals turned
the exercise wheel. The low-casein animals 12 exercised about twice as
much, when measured over a two-week period! This observation seems
to be very similar to how one feels after eating a high-protein meal: slug-
gish and sleepy. I have heard that a side effect of the protein-drenched
Atkins Diet is fatigue. Have you ever noticed this feeling in yourself
after a high-protein meal?

APPENDIX B

Experimental
Design of the China Study

Sixty-five counties in twenty-four different provinces (out of twenty-
seven) were selected for the survey. They represented the full range
of mortality rates for seven of the more common cancers. They also
provided broad geographic coverage and were within four hours' travel
time of a central laboratory. The survey counties represented:

• semitropical coastal areas of southeast China;

• frigid wintry areas in northeast China, near Siberia;

• areas near the Great Gobi desert and the northern steppes;

• and areas near or in the Himalaya Mountains ranging from the far
northwest to the far southwest part of the country.

Except for suburban areas near Shanghai, most counties were located
in rural China where people lived in the same place their entire lives
and consumed locally produced food. Population densities varied wide-
ly, from 20,000 nomadic residents for the most remote county near the
Great Gobi desert, to 1.3 million people for the county on the outskirts
of Shanghai.

This survey is referred to as an ecological or correlation study design,
meaning that we are comparing diet, lifestyle and disease characteristics
of a number of sample populations, in this case the sixy-five counties.
We determine how these characteristics, as county averages, correlate

353

354

THE CHINA STUDY

or associate with each other. For example, how does dietary fat relate to
breast cancer rates? Or how does blood cholesterol relate to coronary
heart disease? How does a certain kind of fatty acid in red blood cells
relate to rice consumption? We could also compare blood testosterone
levels or estrogen levels with breast cancer risk. We did thousands of
different comparisons of this type.

In a study of this kind, it is important to note that only the average
values for county populations are being compared. Individuals are not
being compared with individuals (in reality, neither does any other epi-
demiological study design). As ecological studies go, this study, with its
sixy-five counties, was unusually large. Most such studies only have ten
to twenty such population units, at most.

Each of the sixty-five counties provided 100 adults for the survey.
One-half were male and one-half female, all aged thirty-five to sixty-
four years. The data were collected in the following manner:

• each person volunteered a blood sample and completed a diet and
lifestyle questionnaire;

• one-half of the people provided a urine sample;

• the survey teams went to 30% of the homes to carefully measure
food consumed by the family over a three-day period;

• samples of food representing the typical diets at each survey site
were collected at the local marketplace and were later analyzed for
dietary and nutritional factors.

One of the more important questions during the early planning
stages was how to survey for diet and nutrition information. Estimating
consumption of food and nutrients from memory is a common method,
but this is very imprecise, especially when mixed dishes are consumed.
Can you remember what foods you ate last week, or even yesterday?
Can you remember how much? Another even more crude method of
estimating food intake is to see how much of each food is sold in the
marketplace. These findings can give reasonable estimates of diet trends
over time for whole populations, but they do not account for food waste
or measure individual amounts of consumption.

Although each of these relatively crude methods can be useful for
certain purposes, they still are subject to considerable technical error
and personal bias. And the bigger the technical error, the more difficult
it is to detect significant cause-effect associations.

We wanted to do better than crudely measure which foods and how

EXPERIMENTAL DESIGN OF THE CHINA STUDY

355

much of these foods were being consumed. Thus we decided to evaluate
nutritional conditions by analyzing blood and urine samples for indica-
tors (biomarkers) of multiple nutrient intakes. These analyses would be
far more objective than having people recall what they ate.

Collecting and analyzing blood, however, was not easy to arrange, at
least not in the way that we preferred. The initial problem was getting
enough blood. For cultural reasons, rural Chinese were reluctant to pro-
vide blood samples. A finger prick seemed to be the only possibility but
this was not good enough. A regular vial of blood would give 100 times
as much blood and allow for analyses of many more factors.

Dr. Junshi Chen of our team, at the Institute of Nutrition and Food
Hygiene in the Ministry of Health, had the unenviable task of convinc-
ing these volunteers to give a regular vial of blood. He succeeded. Sir
Richard Peto at the University of Oxford of our team then made the very
practical suggestion of combining the individual blood samples to make
a big pool of blood for each village for each sex. This strategy gave more
than 1,200-1,300 times more blood when compared with the finger
prick method.

Making big pools of blood had enormous implications and made
possible the China Study, as it later became known. It allowed analyses
of far more indicators of diet and health. This allowed us to consider
relationships in a far more comprehensive manner than would have
otherwise been possible. For more detail on the theoretical and practical
basis for collecting and analyzing blood in this way the reader is referred
to the original monograph of the study. 1

After collecting the blood, we then had to decide who would do the
many analyses that were possible. We wanted nothing but the best.
While some analyses were conducted at our Cornell lab and at Dr.
Chen's Beijing lab, the rest of the analyses, especially the more special-
ized types, were done in about two dozen laboratories located in six
countries and in four continents. Laboratories were selected because of
their demonstrated expertise and interest. The laboratory participants
are listed in the original monograph. 1

HOW GOOD IS THIS STUDY?

Because this survey was a one-of-a-kind opportunity we intended that
it be the best of its kind ever undertaken. It was comprehensive; it was
high quality; and its uniqueness allowed new opportunities to inves-
tigate diet and disease that were never before possible. These features

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THE CHINA STUDY

of comprehensiveness, quality and uniqueness greatly improved the
credibility and reliability of the findings — by far. Indeed, the New York
Times, in a lead story in its Science Section, called the study "The Grand
Prix" of epidemiological studies.

COMPREHENSIVENESS OF DATA

This survey was, and still is, the most comprehensive of its kind ever
undertaken. After all the blood, urine and food samples were collected,
stored and analyzed, and after the final results were tabulated and evalu-
ated for quality (a few suspect results were not included in the final
publication), we were able to study 367 variables. These represented
a wide variety of dietary, lifestyle and disease characteristics, now in-
cluded in a dense 896-page monograph. 1 There were:

• disease mortality rates on more than forty-eight different kinds of
disease 2 ;

• 109 nutritional, viral, hormonal and other indicators in blood;

• over twenty-four urinary factors;

• almost thirty-six food constituents (nutrients, pesticides, heavy
metals);

• more than thirty-six specific nutrient and food intakes measured in
the household survey;

• sixty diet and lifestyle factors obtained from questionnaires;

• and seventeen geographic and climatic factors.

The study was comprehensive, not only because of the sheer number
of variables, but also because most of these variables varied over broad
ranges, as with the cancer mortality rates. Broad ranges strengthened
our ability to detect important previously undiscovered associations of
variables.

QUALITY OF DATA

A number of features added quality to this study.

• The adults chosen for this survey were limited to those who were
thirty-five to sixty-four years of age. This is the age range in which
the diseases being investigated are more common. Information on
death certificates of people older than sixty-four years was not in-
cluded in the survey because this information was considered less
reliable.

EXPERIMENTAL DESIGN OF THE CHINA STUDY

357

• In each of the sixty-five counties in the study, two villages were
selected for the collection of the information. Having two villages
in each county rather than one gives a more reliable county av-
erage. When the values of two villages are more similar to each
other than to all the other counties, then this means higher-quality
data. 3

• When possible, variables were measured by more than one kind
of method. For example, iron status was measured in six different
ways, riboflavin (vitamin B 2 ) in three ways, and so forth. Also, in
many cases, we could assess the quality and reliability of data by
comparing variables known to have plausible biological relation-
ships.

• The populations under study proved to be very stable. An average
of 93-94% of the men in the survey were born in the county where
they lived at the time of the survey; for women it was 89%. Also,
according to data published by the World Bank, 4 the diets at the
time of our survey were very similar to those consumed in earlier
years. This was ideal because those earlier years represented the
time when the diseases were initially forming.

UNIQUENESS OF DATA

One idea that makes our study unique is our use of the ecologic study
design. Critics of the ecologic study design correctly assume that it is a
weak design for determining cause-and-effect associations when one is
interested in the effects of single causes acting on single outcomes. But
this is not the way that nutrition works. Rather, nutrition causes or pre-
vents disease by multiple nutrients and other chemicals acting together,
as in foods. An ecologic study is almost ideal if we wish to learn how
an array of dietary factors act together to cause disease. It is the com-
prehensive effects of nutrients and other factors on disease occurrence
where the most important lessons are to be learned. To investigate these
comprehensive causes of disease, it was therefore necessary to record
as many dietary and other lifestyle factors as possible, then formulate
hypotheses and interpret data that represent comprehensiveness.

Perhaps the most unique characteristic that set this study apart con-
cerned the nutritional characteristics of the diets consumed in rural
China. Virtually every other human study on diet and health, of what-
ever design, has involved subjects who were consuming a rich Western

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THE CHINA STUDY

diet. This is true even when vegetarians are included in the study be-
cause 90% of vegetarians still consume rather large amounts of milk,
cheese and eggs, while a significant number still consume some fish
and poultry. As is shown in the accompanying chart (Chart B.l), 5 there
is only a small difference in the nutritional properties of non-vegetarian
and vegetarian diets as consumed in Western countries.

CHART B.l: VEGETARIAN AND NON-VEGETARIAN DIET
COMPARISONS AMONG WESTERNERS

Nutrient

Vegetarian

Non-vegetarian

Fat (% of calories)

30-36

34-38

Cholesterol (g/day)

150-300

300-500

Carbohydrates (% of calories)

50-55

<50

Total protein (% of calories)

12-14

14-18

Animal protein (% of total protein)

40-60

60-70

A strikingly different dietary situation existed in China. In America,
15-17% of our total calories is provided by protein, and upwards of 80%
of this amount is animal-based. In other words, we gorge on protein and
we get most of it from meat and dairy products. But in rural China, they
consume less protein overall (9-10% of total calories), and only 10%
of it comes from animal-based foods. This means that there are many
other major nutritional differences in the Chinese and American diets,
as shown in Chart B.2. 1

CHART B.2: CHINESE AND AMERICAN DIETARY INTAKES

Nutrient

China

United States

Calories (kcal/kg body wt./day)

40.6

30.6

Total fat (% of calories)

14.5

34-38

Dietary fiber (g/day)

Total protein (g/day)

Animal protein (% of total calories)

0.8*

10-1 1

Total iron (mg/day)

* Non-fish animal protein

EXPERIMENTAL DESIGN OF THE CHINA STUDY

359

This was the first and only large study that investigated this range of
dietary experience and its health consequences. Chinese diets ranged
from rich to very rich in plant-based foods. In all other studies done on
Western subjects, diets ranged from rich to very rich in animal-based
foods. It was this distinction that made the China Study so different
from other studies.

MAKING IT HAPPEN

Organization and conduct of a study of this size, scope and quality was
possible because of the exceptional skills of Dr. Junshi Chen. Survey
sites were scattered across the far reaches of China. In American travel
distances, they ranged from the Florida Keys to Seattle, Washington,
and from San Diego, California, to Bangor, Maine. Travel between these
places was more difficult than in the United States, and supplies and
instructions for the survey had to be in place and standardized for all
collection sites. And this was done before e-mails, fax machines and cel-
lular phones were available.

It was important that the twenty-four provincial health teams, each
comprised of twelve to fifteen health workers, be trained to carry out
the blood, food and urine collections and complete the questionnaires
in a systematic and standardized manner. To standardize the collection
of information, Dr. Chen divided the country into regions. Each region
sent trainers to Beijing for the senior training session. They, in turn, re-
turned to their home provinces to train the provincial health teams.

Although the U.S. National Cancer Institute (NCI) of the National
Institutes of Health (NIH) provided the initial funding for this project,
the Chinese Ministry of Health paid the salaries of the approximately
350 health workers. It is my estimate that the Chinese contribution to
the project was approximately $5-6 million. This compares with the
U.S. contribution of about $2.9 million over a ten-year period. Were
the U.S. government to have paid for this service in a similar project in
the U.S., it would have cost at least ten times this amount, or $50-60
million.

APPENDIX C

The "Vitamin" D Connection

The most impressive evidence favoring plant-based diets is the way that
so many food factors and biological events are integrated to maximize
health and minimize disease. Although the biological processes are ex-
ceptionally complex, these factors still work together as a beautifully
choreographed, self-correcting network. It is exceptionally impressive,
especially the coordination and control of this network.

Perhaps a couple of analogies might help to illustrate such a process.
Flocks of birds in flight or schools of fish darting about are able to shift
direction in a microsecond without bumping into each other. They
seem to have a collective consciousness that knows where they are go-
ing and when they will rest. Colonies of ants and swarms of bees also
integrate varying labor chores with great proficiency. But as amazing
as these animal activities are, have you ever thought about how their
behaviors are coordinated with such finesse? I see these same charac-
teristics, and more, in the way that the countless factors of plant-based
foods work their magic to create health at all levels within our body,
among our organs and between our cells and among the enzymes and
other sub-cellular particles within our cells.

For those unfamiliar with biomedical research laboratories, the walls
of these labs are often covered with large posters showing thousands of
biochemical reactions operating within our bodies. These are reactions
that are known; far more remain to be discovered. The interdependence
of these reactions with each other is especially informative, even awe-
some in its implications.

361

362

THE CHINA STUDY

An example of a very small portion of this enormous network of re-
actions is the effect of vitamin D and its metabolites on several of the
diseases discussed in this book. This particular network illustrates a com-
plex interconnection between the inner workings of our cells, the food we
eat and the environment in which we live (Chart C.l). Although some of
the vitamin D present in our bodies may come from food, we can usually
get all that we need from a few hours of sunshine each week. In fact, it
is our ability to make our vitamin D that leads to the idea that it is not a
vitamin; it is a hormone (i.e., made in one part of our body but function-
ing in another part). The sun's UV rays make vitamin D from a precursor
chemical located in our skin. Provided we get adequate sunshine, this is
all the vitamin D we need. 1 We can, of course, also get vitamin D from
fortified milk, certain fish oils and some vitamin supplements.

The vitamin D made in our skin then travels to our liver, where it is
converted by an enzyme to a vitamin D metabolite. This metabolite's
main function is to serve as the body's storage form of vitamin D (while
remaining mostly in the liver but also in body fat).

The next step is the crucial one. When needed, some of the stor-
age form of vitamin D in the liver is transported to the kidney, where
another enzyme converts it into a supercharged vitamin D metabolite,
which is called 1,25 D. The rate at which the storage form of vitamin
D is converted to the supercharged 1,25 D is a crucial reaction in this
network. The 1,25 D metabolite does most of the important work of
vitamin D in our bodies.

This supercharged 1,25 D is about 1,000 times more active than the
storage vitamin D. Supercharged 1,25 D only survives for six to eight
hours once it is made. In contrast, our storage vitamin D survives for
twenty days or more. 2, 3 This demonstrates an important principle typi-
cally found in networks like this: the far greater activity, the far shorter
lifetime and the far lower amounts of the 1,25 D end product provide a
very responsive system wherein the 1,25 D can quickly adjust its activi-
ty minute-by-minute and microsecond-by-microsecond as long as there
is sufficient storage vitamin D to draw from. Small changes, making a
big difference, can occur quickly.

The relationship between the storage form of vitamin D and the
supercharged 1,25 D is like having a large tank of natural gas buried
in our yard (storage vitamin D) but carefully using only a very tiny
amount of gas to light the burner at our stovetop. It is critical that the
amount and timing of gas (1,25 D) coming to our stovetop be carefully

THE "VITAMIN" D CONNECTION 363

CHART C.l: THE VITAMIN D NETWORK

regulated, regardless of how much there may be in the tank, whether it
is low or whether it is full. However, it is also useful that we maintain
an adequate supply in our storage tank. In the same way, it is critical
that the kidney enzyme in this reaction has a soft, sensitive touch, so to
speak, as it produces the right amount of the 1,25 D at the right time for
its very important work.

One of the more important things that vitamin D does, mostly
through its conversion to supercharged 1,25 D, is to control the devel-
opment of a wide variety of serious diseases. For the sake of simplicity,
this is schematically represented by showing the inhibition of the con-
version of healthy tissue to diseased tissue by 1,25 D. 4-12

So far, we can see how adequate sunshine exposure, by ensuring
enough storage form of vitamin D, helps to prevent cells from becom-
ing diseased. This suggests that certain diseases might be more common
in areas of the world where there is less sunshine, in countries nearer
the North and South Poles. Indeed there is such evidence. To be more
specific: in the northern hemisphere, communities that are farther north
tend to have more Type 1 diabetes, multiple sclerosis, rheumatoid arthritis,
osteoporosis, breast cancer, prostate cancer and colon cancer, in addition to
other diseases.

Researchers have known for eighty years that multiple sclerosis,
for example, is associated with increasing latitude. 13 As you can see in
Chart C.2, there is a huge difference in MS prevalence as one goes away
from the equator, being over 100 times more prevalent in the far north
than at the equator. 14 Similarly, in Australia, there is less sunshine and

364

THE CHINA STUDY

more MS as one goes farther south (r=91%). 15 MS is about sevenfold
greater in southern (43°S) than in northern Australia (19°S). 16

A lack of sunshine, however, is not the only factor related to these
diseases. There is a larger context. The first thing to note is the control
and coordination of these vitamin D-related reactions. Control operates
at several places in this network, but, as I already said, it is the conver-
sion of storage vitamin D into the supercharged 1,25 D in the kidneys
that is especially critical. In considerable measure, this control is exer-
cised by another complex network of reactions involving a "manager"-
type hormone produced by the parathyroid gland located in our neck
(Chart C.3).

When, for example, we need more 1,25 D, parathyroid hormone in-
duces the kidney enzyme activity to produce more 1,25 D. When there
is enough 1,25 D, parathyroid hormone slows down the kidney enzyme

THE "VITAMIN" D CONNECTION

365

activity. Within seconds, parathyroid hormone manages how much 1,25
D there will be at each time and place. Parathyroid hormone also acts as
a conductor at several other places in this network, as shown by the sev-
eral arrows. By being aware of the role of each player in its "orchestra,"
it coordinates, controls and finely tunes these reactions as a conductor
would a symphony orchestra.

Under optimal conditions, sunshine exposure alone can supply all
the vitamin D that we need to produce the all-important 1 ,25 D at the
right time. Even the elderly, who are not able to produce as much vita-
min D from sunshine, have nothing to worry about if there is enough
sunshine. 17 How much is "enough"? If you know how much sunshine
causes a slight redness of your skin, then one-fourth of this amount,
provided two to three times per week, is more than adequate to meet
our vitamin D needs and to store some in our liver and body fat. 17 If
your skin becomes slightly red after about thirty minutes in the sun,
then ten minutes, three times per week will be enough exposure to get
plenty of vitamin D.

When and if we don't get enough sunshine, it may be helpful to con-
sume vitamin D from our diets. Almost all of the vitamin D found in our
diet has been artificially added to foods like milk and breakfast cereals.
Along with vitamin supplements, this amount of vitamin D can be quite
significant and, under certain circumstances, there is some evidence
that this practice may be beneficial. 18 " 21

In this scheme, sunshine and parathyroid hormone work together in
a marvelously coordinated way to keep this system running smoothly,
both in filling our vitamin D tank and in helping to produce from mo-
ment to moment the exact amount of 1,25 D that we need. When it
comes to getting sufficient sunshine or getting vitamin D in food, taking
light from the sun makes far more sense.

THROWING WRENCHES INTO THE SYSTEM

There are several studies now showing that if 1,25 D remains at con-
sistently low levels, the risk of several diseases increases. So then the
question is: what causes low levels of 1,25 D? Animal protein-contain-
ing foods cause a significant decrease in 1,25 D. 22 These proteins create
an acidic environment in the blood that blocks the kidney enzyme from
producing this very important metabolite. 23

A second factor that influences this process is calcium. Calcium in
our blood is crucial for optimum muscle and nerve functioning, and it

366

THE CHINA STUDY

CHART C.3: ROLE OF THE PARATHYROID HORMONE
IN THE REGULATION OF SUPERCHARGED 1,25 D

must be maintained within a fairly narrow range. The 1,25 D keeps the
blood levels of calcium operating within this narrow range by moni-
toring and regulating how much calcium is absorbed from food being
digested in the intestine, how much calcium is excreted in the urine and
feces and how much is exchanged with the bone, the big supply tank
for the body's calcium. For example, if there is too much calcium in the
blood, 1,25 D becomes less active, less calcium is absorbed and more
calcium is excreted. It is a very sensitive balancing act in our bodies.
As blood calcium goes up, 1,25 D goes down, and when blood calcium
goes down, 1,25 D goes up. 10 24 Here's the kicker: if calcium consump-
tion is unnecessarily high, it lowers the activity of the kidney enzyme
and, as a consequence, the level of 1,25 D. 125 In other words, routinely
consuming high-calcium diets is not in our best interests.

The blood levels of 1,25 D therefore are depressed both by consum-
ing too much animal protein and too much calcium. Animal-based
food, with its protein, depresses 1,25 D. Cow's milk, however, is high
both in protein and calcium. In fact, in one of the more extensive stud-
ies on MS that is associated with lower levels of 1,25 D, cow's milk
was found to be as important a factor as latitude mentioned earlier. 26
For example, the association of MS with latitude and sunshine shown
in Chart C.2 also is seen with animal-based foods shown in Chart
C.4. 14

One could hypothesize that diseases like MS are due, at least in part,
to a lack of sunshine and lower vitamin D status. This is supported by the
observation that northern people living along coastlines (e.g., Norway

THE "VITAMIN" D CONNECTION

367

and Japan) 26 who consume lots of vitamin D-rich fish have less MS than
people living inland. However, in these fish-eating communities with
lower rates of disease, much less cow's milk is consumed. Consuming
cow's milk has been shown to associate with MS 26 and Type 1 diabetes 27
independent of fish intake.

In another reaction associated with this network, increased intakes
of animal protein also enhance the production of insulin-like growth
factor (IGF-1, first introduced in chapter eight) and this enhances
cancer cell growth. 5 In effect, there are many reactions acting in a co-
ordinated and mutually consistent way to cause disease when a diet
high in animal protein is consumed. When blood levels of 1,25 D are
depressed, IGF-1 simultaneously becomes more active. Together, these
factors increase the birth of new cells while simultaneously inhibit-
ing the removal of old cells, both favoring the development of cancer
(seven studies cited by 28 ). For example, people with higher-than-nor-
mal blood levels of IGF-I have been shown to have 5.1 times the risk of

CHART C.4: WORLDWIDE DISTRIBUTION OF CALORIE CONSUMPTION
FROM ANIMAL-BASED FOODS FOR 120 COUNTRIES 14

South 40 30 20 10 0 10 20 30 40 North
Latitude Latitude

Degrees Latitude

368

THE CHINA STUDY

advanced-stage prostate cancer. 28 If combined with low blood levels of
a protein that inactivates IGF-I 29 (i.e., more IGF-1 activity), there is 9.5
times the risk of advanced- stage prostate cancer. 18 This level of disease risk
is alarming. Fundamental to it all is the fact that animal-based foods like
meat and dairy 30-32 lead to more IGF-I and less 1,25 D, both of which
increase cancer risk.

These are only a few of the factors and events associated with this
vitamin D network. With the right food and environment, these events
and reactions cooperate in an integrated manner to produce health ben-
efits. In contrast, when the wrong food is consumed, its adverse effects
are mediated by not one, but many, of the reactions within this network.
Also, many factors in such foods, even beyond the protein and calcium,
participate in causing the problem. And, finally, it often is not one dis-
ease but many that are likely to occur.

What impresses me about this and other networks is the convergence
of so many disease-causing factors operating through so many different
reactions to produce a common result. When that common result is
more than one disease, it is even more impressive. When these various
factors are found in one type of food and this food is epidemiologi-
cally related to one or more of these diseases, the associations become
still more impressive. This example begins to explain why dairy foods
would be expected to increase the risk of these diseases. There is no
way that so many intricate mechanisms, operating in such synchrony to
produce the same result, are only a random unimportant happenstance.
Nature would not have been so devious as to refine such a useless in-
ternally conflicting maze. Networks like this exist throughout the body
and within the cells. But of even more importance, they are highly inte-
grated into a far larger dynamic called "life."

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PART I

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Chapter 2

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Chapter 3

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17. If this defect becomes part of the first round of daughter cells, then this will be passed on to
all subsequent generations of cells, with the potential to eventually become clinically detect-
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required to initiate and promote cancer, and 2) not all genetic defects result in cancer.

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42. Schulsinger DA, Root MM, and Campbell TC. "Effect of dietary protein quality on develop-
ment of aflatoxin Bl-induced hepatic preneoplastic lesions." J. Natl. Cancer Inst. 81 (1989):
1241-1245.

43. Youngman LD. The growth and development of aflatoxin Bl-induced preneoplastic lesions, tu-
mors, metastasis, and spontaneous tumors as they are influenced by dietary protein level, type, and
infervenfion. Ithaca, NY: Cornell University, Ph.D. Thesis, 1990.

44. Beasley RE "Hepatitis B virus as the etiologic agent in hepatocellular carcinoma-epidemio-
logic considerations." Hepatol. 2 (1982): 21S-26S.

45. Blumberg BS, Larouze B, London WT, et al. "The relation of infection with the hepatitis B
agent to primary hepatic carcinoma." Am. J. Pathol. 81 (1975): 669-682.

46. Chisari FV, Ferrari C, and Mondelli MU. "Hepatitis B virus structure and biology." Microbiol.
Pafhol. 6 (1989): 311-325.

47. Hu J, Cheng Z, Chisari FX et al. "Repression of hepatitis B virus (HBV) transgene and HBV-
induced liver injury by low protein diet." Oncogene 15 (1997): 2795-2801.

48. Cheng Z, Hu J, KingJ, et al. "Inhibition of hepatocellular carcinoma development in hepatitis
B virus transfected mice by low dietary casein." Hepatology 26 (1997): 1351-1354.

49. Hawrylewicz EJ, Huang HH, Kissane JQ, et al. "Enhancement of the 7,12-dimethylbenz(a)a
nthracene (DMBA) mammary tumorigenesis by high dietary protein in rats." Nutr. Reps. Int.
26 (1982): 793-806.

374

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50. Hawrylewicz EJ. "Fat-protein interaction, defined 2-generation studies." In: C. Ip, D. E Bin,
A. E. Rogers and C. Mettlin (eds.), Dietary fat and cancer, pp. 403-434. New York: Alan R.
Liss, Inc., 1986.

51. Huang HH, Hawrylewicz EJ, Kissane JQ, et al. "Effect of protein diet on release of prolactin
and ovarian steroids in female rats." Nutr: Rpls. Int. 26 (1982): 807-820.

52. O'Connor TP, Roebuck BD, and Campbell TC. "Dietary intervention during the post-dosing
phase of L-azaserine-induced preneoplastic lesions. "J Natl Cancer Inst 75 (1985): 955-957.

53. O'Connor TP, Roebuck BD, Peterson F, et al. "Effect of dietary intake of fish oil and fish pro-
tein on the development of L-azaserine-induced preneoplastic lesions in rat pancreas." J Natl
Cancer Inst 75 (1985): 959-962.

54. He Y. Effects of carotenoids and dietary carotenoid extracts on aflatoxin B t -induced mutagenesis
and hepatocarcinogenesis. Ithaca, NY: Cornell University, PhD Thesis, 1990.

55. He Y, and Campbell TC. "Effects of carotenoids on aflatoxin B,-induced mutagenesis in S.
typhimurium TA 100 and TA 98." Nutr: Cancer 13 (1990): 243-253.

Chapter 4

1. Li J-Y, Liu B-Q, Li G-Y, et al. "Atlas of cancer mortality in the People's Republic of China. An
aid for cancer control and research." Int. J. Epid. 10 (1981): 127-133.

2. Higginson J. "Present trends in cancer epidemiology." Proc. Can. Cancer Conf. 8 (1969):
40-75.

3. Wynder EL, and Gori GB. "Contribution of the environment to cancer incidence: an epide-
miologic exercise." J. Natl. Cancer Inst. 58 (1977): 825-832.

4. Doll R, and Peto R. "The causes of cancer: Quantitative estimates of avoidable risks of cancer
in the Unites States today." J Natl Cancer Inst 66 (1981): 1192-1265.

5. Fagin D. News release. "Breast cancer cause still elusive study: no clear link between pollution,
breast cancer on LI." August 6, 2002. Newsday.com. Accessed at httpyAvww.newsday.com/news/
local/longisland/ny-licanc062811887aug06.story?coll=ny%2Dtop%2Dheadlines

6. There were 82 mortality rates, but about a third of these rates were duplicates of the same
disease for different aged people.

7. Calorie intake in China is for a 65 kg adult male doing "light physical work." Comparable
data for the American male is adjusted for a body weight of 65 kg.

8. SerVaas C. "Diets that protected against cancers in China." The Saturday Evening Post October
1990: 26-28.

9. All the available disease mortality rates were arranged in a matrix so that it was possible
to readily determine the relationship of each rate with every other rate. Each comparison
was then assigned a plus or minus, depending on whether they were directly or inversely
correlated. All plus correlations were assembled in one list and all minus correlations were
assembled in a second list. Each individual entry in either list was therefore positively related
to entries in its own list but inversely related to diseases in the opposite list. Most, but not all,
of these correlations were statistically significant.

10. Campbell TC, Chen J, Brun T, et al. "China: from diseases of poverty to diseases of affluence.
Policy implications of the epidemiological transition." Eco!. Food Nutr. 27 (1992): 133-144.

11. Chen J, Campbell TC, Li J, et al. Diet, !i/e-style and mortality in China. A study of the character-
istics of 65 Chinese counties. Oxford, UK; Ithaca, NY; Beijing, PRC: Oxford University Press;
Cornell University Press; People's Medical Publishing House, 1990.

12. Lipid Research Clinics Program Epidemiology Committee. "Plasma lipid distributions in
selected North American Population. The Lipid Research Clinics Program Prevalence Study."
Circulation 60 (1979): 427-439.

13. Campbell TC, Parpia B, and Chen J. "Diet, lifestyle, and the etiology of coronary artery dis-
ease: The Cornell China Study." Am. J. Cardiol 82 (1998): 18T-21T.

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14. These data are for villages SA, LC and RA for women and SA, QC and NB for men, as seen in
the monograph (Chen, et al. 1990)

15. Sirtori CR, Noseda G, and Descovich GC. "Studies on the use of a soybean protein diet for
the management of human hyperlipoproteinemias." In: M. J. Gibney and D. Kritchevsky
(eds.), Current Topics in Nutrition and Disease, Volume 8: Animal and Vegetable Proteins in Lipid
Metabolism and Atherosclerosis., pp. 135-148. New York, NY: Alan R. Liss, Inc., 1983.

16. Carroll KK. "Dietary proteins and amino acids — their effects on cholesterol metabolism." In.
M. J. Gibney and D. Kritchevsky (eds.), Animal and Vegetable Proteins in Lipid Metabolism and
Atherosclerosis, pp. 9-17. New York, NY: Alan R. Liss, Inc., 1983.

17. Terpstra AHM, Hermus RJJ, and West CE. "Dietary protein and cholesterol metabolism in
rabbits and rats." In: M.J. Gibney and D. Kritchevsky (eds.). Animal and Vegetable Proteins in
Lipid Metabolism and Athersclerosis, pp. 19-49. New York: Alan R. Liss, Inc., 1983.

18. Kritchevsky D, Tepper SA, Czarnecki SK, et al. "Atherogenicity of animal and vegetable pro-
tein. Influence of the lysine to arginine ratio." Atherosclerosis 41 (1982): 429^f31.

19. Dietary fat can be expressed as percent of total weight of the diet or as percent of total calo-
ries. Most commentators and researchers express fat as percent of total calories because we
primarily consume food to satisfy our need for calories, not our need for weight. I will do the
same throughout this book.

20. National Research Council. Diet, Nutrition and Cancer. Washington, DC: National Academy
Press, 1982.

21. United States Department of Health and Human Services. The Surgeon General's Report on
Nutrition and Health. Washington, DC: Superintendant of Documents, U.S. Government
Printing Office, 1988.

22. National Research Council, and Committee on Diet and Health. Diet and health: implications
for reducing chronic disease risk. Washington, DC: National Academy Press, 1989.

23. Expert Panel. Food, nutrition and the prevention of cancer, a global perspective. Washington,
DC: American Institute for Cancer Research/World Cancer Research Fund, 1997.

24. Exceptions include those foods artificially stripped of their fat, such as non-fat milk.

25. Armstrong D, and Doll R. "Environmental factors and cancer incidence and mortality in
different countries, with special reference to dietary practices." Int. ]. Cancer 15 (1975):
617-631.

26. U.S. Senate. "Dietary goals for the United States, 2nd Edition." Washington, DC: U.S. Gov-
ernment Printing Office, 1977.

27. Committee on Diet Nutrition and Cancer. Diet, nutrition and cancer: directions for research.
Washington, DC: National Academy Press, 1983.

28. There also were a number of other policy statements and large human studies that were
begun at about this time that were to receive much public discussion and that were founded
and/or interpreted in relation to dietary fat and these diseases. These included the initiation
of the U.S. Dietary Guidelines report series begun in 1980, the Harvard Nurses' Health Study
in 1984, the initial reports of the Framingham Heart Study in the 1960s, the Seven Countries
Study of Ancel Keys, the Multiple Risk Factor Intervention Trial (MRFIT) and others.

29. Carroll KK, Braden LM, Bell JA, et al. "Fat and cancer." Cancer 58 (1986): 1818-1825.

30. Drasar BS, and Irving D. "Environmental factors and cancer of the colon and breast." Br J.
Cancer 27 (1973): 167-172.

31. Haenszel W, and Kurihara M. "Studies of Japanese Migrants: mortality from cancer and other
disease among Japanese and the United States." J Natl Cancer Inst 40 (1968): 43-68.

32. Higginson J, and Muir CS. "Epidemiology in Cancer." In: J. E Holland and E. Frei (eds.),
Cancer Medicine, pp. 241-306. Philadelphia, PA: Lea and Febiger, 1973.

33. The correlation of fat intake with animal protein intake is 84% for grams of fat consumed and
70% for fat as a percent of calories.

376

THE CHINA STUDY

34. KelseyJL, Gammon MD, and Esther MJ. "Reproductive factors and breast cancer." Epidemiol
Revs. 15 (1993): 36-47.

35. de Stavola BL, Wang DY, Allen DS, et al. "The association of height, weight, menstrual and
reproductive events with breast cancer: results from two prospective studies on the island of
Guernsey (United Kingdom)." Cancer Causes and Control 4 (1993): 331-340.

36. Rautalahti M, Albanes D, VirtamoJ, et al. "Lifetime menstrual activity — indicator of breast
cancer risk." (1993): 17-25

37. It was not possible to statistically detect an association of blood hormone levels with breast
cancer risk within this group of women because their blood samples were taken at random
times of their menstrual cycles and breast cancer rates were so low, thus minimizing the abil-
ity to detect such an association, even when real.

38. Key TJA, Chen J, Wang DY, et al. "Sex hormones in women in rural China and in Britain."
Brit.]. Cancer 62 (1990): 631-636.

39. These biomarkers include plasma copper, urea nitrogen, estradiol, prolactin, testosterone
and, inversely, sex hormone binding globulin, each of which has been known to be associated
with animal protein intake from previous studies.

40. For the total dietary fiber (TDF), the averages for China and the U.S. were 33.3 and 11.1
grams per day, respectively. The range of the county averages are 7.7-77.6 grams per day in
China, compared with a range of 2.4-26.6 grams per day for the middle 90% of American
males.

41. The correlation for plant protein was +0.53*** and for animal protein was +0.12.

42. In principle, using "cancer prevalence within families" as the outcome measurement more ef-
fectively controls for the various causes of cancer that associate with different kinds of cancer,
thus permitting study of an isolated effect of the dietary factor.

43. Guo W, Li J, Blot WJ, et al. "Correlations of dietary intake and blood nutrient levels with
esophageal cancer mortality in China." Nutr. Cancer 13 (1990): 121-127.

44. The full effects of these fat-soluble antioxidants can be demonstrated only when antioxidant
concentrations are adjusted for the levels of LDL for individual subjects. This was not known
at the time of the survey, thus provisions were not made for this adjustment.

45. Kneller RW, Guo W Hsing AW, et al. "Risk factors for stomach cancer in sixty-five Chinese
counties." Cancer Epi. Biomarkers Prev. 1 (1992): 113-118.

46. Information Plus. Nutrition: a key to good health. Wylie, TX: Information Plus, 1999.

47. Westman EC, Yancy WS, Edman JS, et al. "Carbohydrate Diet Program." Am.]. Med. 113
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48. Atkins RC. Dr. Atkins' New Diet Revolution. New York, NY: Avon Books, 1999.

49. Wright JD, Kennedy-Stephenson J, Wang CY, et al. "Trends in Intake of Energy and Macro-
nutrients — United States, 1971-2000." Morbidity and mortality weekly report 53 (February 6,
2004): 80-82.

50. Noakes M, and Clifton PM. "Weight loss and plasma lipids." Curr. Opin. Lipidol. 11 (2000):
65-70.

51. Bilsborough SA, and Crowe TC. "Low-carbohydrate diets: what are the potential short- and
long-term health implications?" Asia Pac.J. Clin. Nutr. 12 (2003): 396-404.

52. Stevens A, Robinson DP, TurpinJ, et al. "Sudden cardiac death of an adolescent during diet-
ing." South. Med. J. 95 (2002): 1047-1049.

53. Patty A. "Low-carb fad claims teen's life - Star diet blamed in death." The Daily Telegraph
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54. Atkins, 1999. Page 275.

55. Atkins claims that an antioxidant cocktail can protect against heart disease, cancer and aging,
a claim refuted by several large trials recently completed (see chapter 1 1).

56. Atkins, 1999. Page 103.

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58. Campbell TC. "Energy balance: interpretation of data from rural China." Toxicological Sci-
ences 52 (1999): 87-94.

59. Horio F, Youngman LD, Bell RC, et al. "Thermogenesis, low-protein diets, and decreased de-
velopment of AFBl-induced preneoplastic foci in rat liver." Nutr. Cancer 16 (1991): 31-41.

60. Krieger E, Youngman LD, and Campbell TC. "The modulation of aflatoxin(AFBl) induced
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61. The cited associations of total animal and plant protein intakes are taken from manuscript
under review

62. Campbell TC, ChenJ, Liu C, et al. "Non-association of aflatoxin with primary liver cancer in
a cross-sectional ecologic survey in the People's Republic of China." Cancer Res. 50 (1990):
6882-6893.

PART II

Chapter 5

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diovascular, Lung, and Blood Diseases." Bethesda, MD: National Institutes of Health, 2002.

3. American Heart Association. "Heart Disease and Stroke Statistics-2003 Update." Dallas, TX:
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4. Braunwald E. "Shattuck lecture-cardiovascular medicine at the turn of the millenium: tri-
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6. Anderson RN. "Deaths: leading causes for 2000." National Vital Statistics Reports 50(16)
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7. Enos WE, Holmes RH, and Beyer J. "Coronary disease among United States soldiers killed in
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8. Esselstyn CJ. "Resolving the coronary artery disease epidemic through plant-based nutri-
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10. Esselstyn CJ. "Lecture: Reversing heart disease." December 5, 2002. Ithaca, NY: Cornell Uni-
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12. Forrester JS, and Shah PK. "Lipid lowering versus revascularization: an idea whose time (for
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13. Now named the National Heart, Lung, and Blood Institute of the National Institutes of Health
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15. Kannel WB, Dawber TR, Kagan A, et al. "Factors of risk in the development of coronary heart
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18. Campbell TC, Parpia B, and Chen J. "Diet, lifestyle, and the etiology of coronary artery dis-
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19. Kagan A, Harris BR, Winkelstein W, et al. "Epidemiologic studies of coronary heart disease
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20. Kato H, Tillotson J, Nichaman MZ, et al. "Epidemiologic studies of coronary heart disease
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21. Morrison LM. "Arteriosclerosis." JAMA 145 (1951): 1232-1236.

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23. Lyon TP, Yankley A, Gofman JW, et al. "Lipoproteins and diet in coronary heart disease."
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24. Gibney MJ, and Kritchevsky D, eds. Current Topics in Nutrition and Disease, Volume 8: Animal
and Vegetable Proteins in Lipid Metabolism and Atherosclerosis. New York, NY: Alan R. Liss,
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25. Sirtori CR, Noseda G, and Descovich GC. "Studies on the use of a soybean protein diet for
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(eds.), Current Topics in Nutrition and Disease, Volume 8: Animal and Vegetable Proteins in Lipid
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26. G.S. Myers, personal communication, cited by Groom, D. "Population studies of atheroscle-
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27. Centers for Disease Control. "Smoking and Health: a national status report." Morbidity and
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28. Centers for Disease Control. "Cigarette smoking among adults — United States, 2000." Mor-
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29. Age-adjusted, ages 25-74.

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31. Page 1319 in Gersh BJ, Braunwald E, and Rutherford JD. "Chronic coronary artery disease."
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33. Shaw PJ, Bates D, Cartlidge NEF, et al. "Early intellectual dysfunction following coronary
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34. Cameron AAC, Davis KB, and Rogers WJ. "Recurrence of angina after coronary artery bypass
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38. Hirshfeld JW, Schwartz JS, Jugo R, et al. "Restenosis after coronary angioplasty: a multivariate
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39. Information Plus. Nutrition: a key to good health. Wylie, TX: Information Plus, 1999.

40. Naifeh SW. The Best Doctors in America, 1994-1995. Aiken, S.C.: Woodward & White, 1994.

41. Esselstyn CB, Jr. "Foreward: changing the treatment paradigm for coronary artery disease."
Am. J. Cardiol 82 (1998): 2T-4T.

42. Esselstyn CB, Ellis SG, Medendorp SV, et al. "A strategy to arrest and reverse coronary artery
disease: a 5-year longitudinal study of a single physicians practice." J. Family Practice 41
(1995): 560-568.

43. Esselstyn CJ. "lntroduction:more than coronary artery disease." Am. J. Cardiol. 82 (1998):
5T-9T.

44. The flow of blood is related to the fourth power of the radius. Thus, a reduction of seven
percent is approximately related to a 30% greater blood flow, although it is not possible to
obtain by calculation a more precise determination of this number.

45. Personal communication with Dr. Esselstyn, 9/15/03.

46. Ornish D, Brown SE, Scherwitz LW, et al. "Can lifestyle changes reverse coronary heart dis-
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47. Ratliff NB. "Of rice, grain, and zeal: lessons from Drs. Kempner and Esselstyn." Cleveland
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48. American Heart Association. "AHA Dietary Guidelines. Revision 2000: A Statement for
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49. National Cholesterol Education Program. "Third report of the National Cholesterol Educa-
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50. Castelli W. "Take this letter to your doctor." Prevention 48 (1996): 61-64.

51. Schuler G, Hambrecht R, Schlierf G, et al. "Regular physical exercise and low-fat diet." Circu-
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Chapter 6

1. Flegal KM, Carroll MD, Ogden CL, et al. "Prevalence and trends in obesity among U.S.
adults, 1999-2000." JAMA 288 (2002): 1723-1727.

2. Ogden CL, Flegal KM, Carroll MD, et al. "Prevalence and trends in overweight among U.S.
children and adolescents." JAMA 288 (2002): 1728-1732.

3. Dietz WH. "Health consequences of obesity in youth: childhood predictors of adult disease."
Pediatrics 101 (1998): 518-525.

4. Fontaine KR, and Barofsky I. "Obesity and health-related quality of life." Obesity Rev. 2
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5. Colditz GA. "Economic costs of obesity and inactivity." Med. Sci. Sports Exerc. 31 (1999):
S663-S667.

6. Adcox S. "New state law seeks to cut down obesity." Jthaca Journal Sept. 21, 2002: 5A.

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8. Berenson, G., Srinivasan, S., Bao, W, Newman, W. P. r., Tracy, R. E., and Wattigney, W. A.
"Association between multiple cardiovascular risk factors and atherosclerosis to children and
young adults. The Bogalusa Heart Study." New Engl. J. Med., 338: 1650-1656, 1998.

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9. Key TJ, Fraser GE, Thorogood M, et al. "Mortality in vegetarians and nonvegetarians: de-
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10. BerganJG, and Brown PT. "Nutritional status of "new" vegetarians." J. Am. Diet. Assoc. 76
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11. Appleby PN, Thorogood M, Mann J, et al. "Low body mass index in non-meat eaters: the
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12. DwyerJT. "Health aspects of vegetarian diets." Am. J. Clin. Nutr. 48 (1988): 712-738.

13. Key TJ, and Davey G. "Prevalence of obesity is low in people who do not eat meat." Brit. Med.
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14. Shintani TT, Hughes CK, Beckham S, et al. "Obesity and cardiovascular risk intervention
through the ad libitum feeding of traditional Hawaiian diet." Am. J. Clin. Nutr. 53 (1991):
1647S-1651S.

15. Barnard RJ. "Effects of life-style modification on serum lipids." Arch. Intern. Med. 151 (1991):
1389-1394.

16. McDougall J, Litzau K, Haver E, et al. "Rapid reduction of serum cholesterol and blood
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491-496.

17. Ornish D, Scherwitz LW, Doody RS, et al. "Effects of stress management training and dietary
changes in treating ischemic heart disease." JAMA 249 (1983): 54-59.

18. Shintani TT, Beckham S, Brown AC, et al. "The Hawaii diet: ad libitum high carbohydrate,
low fat multi-cultural diet for the reduction of chronic disease risk factors: obesity, hyperten-
sion, hypercholesterolemia, and hyperglycemia." Hawaii Med. Journ. 60 (2001): 69-73.

19. Nicholson AS, Sklar M, Barnard ND, et al. "Toward improved management of N1DDM: a ran-
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20. Ornish D, Scherwitz LW, Billings JH, et al. "Intensive lifestyle changes for reversal of coronary
heart disease." JAMA 280 (1998): 2001-2007.

21. Astrup A, Toubro S, Raben A, et al. "The role of low-fat diets and fat substitutes in body
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22. Duncan KH, Bacon JA, and Weinsier RL. "The effects of high and low energy density diets on
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23. Heaton KW. "Food fibre as an obstacle to energy intake." Lancet (1973): 1418-1421.

24. Levin N, Rattan J, and Gilat T. "Energy intake and body weight in ovo-lacto vegetarians." J.
Clin. Gastroenterol. 8 (1986): 451-453.

25. Campbell TC. "Energy balance: interpretation of data from rural China." Toxicological Sci-
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26. Poehlman ET, Arciero PJ, Melby CL, et al. "Resting metabolic rate and postprandial thermo-
genesis in vegetarians and nonvegetarians." Am. J. Clin. Nutr: 48 (1988): 209-213.

27. The study by Poehlman et al. showed high oxygen consumption and higher resting metabolic
rate but was badly misinterpreted by the authors. We had very similar results with experi-
mental rats.

28. Fogelholm M, and Kukkonen-Harjula K. "Does physical activity prevent weight gain — a
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Chapter 8

1. Estrogen present in its free, unbound form.

2. Estrogen activity is due to more than one analogue, but usually refers to estradiol. 1 will use the
general term "estrogen" to include all steroid and related female hormones whose effects paral-
lel estradiol activity. A small amount of testosterone in women also shows the same effect.

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6. Animal protein includes more of the sulphur-containing amino acids. When digested and
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creted by the kidney. A recent report showed a remarkable 84% correlation between animal
protein consumption and urinary acid excretion of sulphate.

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8. Frassetto LA, Todd KM, Morris RC, Jr., et al. "Estimation of net endogenous noncarbonic
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30. This genetically rare type of kidney stone results from an inability of the kidney to reabsorb
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35. Robertson WG, Peacock M, Heybum PJ, et al. "Should recurrent calcium oxalate stone form-
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36. This information was shown in Dr. Robertson's seminar in Toronto.

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38. Cao LC, Boeve ER, de Bruijn WC, et al. "A review of new concepts in renal stone research."
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43. The other four food groups were broccoli, carrot, sweet potato, and winter squash, showing
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proaching or was marginally statistically significant.

44. Berman ER. Biochemistry oj the eye. (Perspectives in vision research). New York, N.Y.: Plenum
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64. This recently published study is more interesting than the others because vitamin E was mea-
sured in a way that is more discriminating by considering the fact that vitamin E is carried in
the blood fat. That is, a high level of blood vitamin E may, at times, be due to high levels of
blood fat. (Am. J. Epidemiol. 150 (1999); 37-44)

65. The effects of vitamin C and selenium in a study by Perkins (Am. J. Epidemiol. 150 (1999):
37-44) were not statistically significant in a logistic regression model, according to the au-
thors. I disagree with their conclusion because the inverse "dose-response" trend (high anti-
oxidant blood levels, less memory loss) was impressive and clearly significant. The authors
failed to address this finding in their analysis.

66. Ortega RM, Requejo AM, Andres P, et al. "Dietary intake and cognitive function in a group of
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67. Perrig WJ, Perrig P, and Stahelin HB. "The relation between antioxidants and memory perfor-
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68. Gale CR, Martyn CN, and Cooper C. "Cognitive impairment and mortality in a cohort of
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70. Jama JW, Launer LJ, Witteman JCM, et al. "Dietary antioxidants and cognitive function in
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71. Martin A, Prior R, Shukitt-Hale B, et al. "Effect of fruits, vegetables or vitamin E-rich diet on
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72. Joseph JA, Shukitt-Hale B, Denisova NA, et al. "Reversals of age-related declines in neuronal
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74. Kalmijn S, Launer LJ, Ott A, et al. "Dietary fat intake and the risk of incident dementia in the
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75. Alzheimer's trend was not statistically significant, perhaps due to the small number of disease
cases.

76. Clarke R, Smith D, Jobst KA, et al. "Folate, vitamin B12, and serum total homocysteine levels
in confirmed Alzheimer disease." Arch. Neurol. 55 (1998): 1449-1455.

77. McCully KS. "Homocysteine theory of arteriosclerosis: development and current status." In:
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78. There is a potential snag in this logic, however. Homocysteine levels are regulated in part by
B vitamins, most notably folic acid and vitamin B 12 , and people who are deficient in these
vitamins may have higher homocysteine levels. People who do not consume animal-based
foods are at risk for having low B 12 levels, and thus high homocysteine levels. However, as
described in chapter eleven, this has more to do with our separation from nature, and not a
deficiency of plant-based diets.

394

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PART III

1. http://www.southbeachdiet.com, accessed 4/26/04

Chapter 1 1

1. Atkins RC. Dr. Atkins' New Diet Revolution. New York, NY: Avon Books, 1999.

2. The Alpha-Tocopherol Beta Carotene Cancer Prevention Study Group. "The effect of vitamin
E and beta carotene on the incidence of lung cancer and other cancers in male smokers." New
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5. Morris CD, and Carson S. "Routine vitamin supplementation to prevent cardiovascular dis-
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6. Kolata G. "Vitamins: more may be too many (Science Section)." The New York Times April 29,
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7. U.S. Department of Agriculture. "USDA Nutrient Database for Standard Reference." Wash-
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9. The exact food listings in the database were: Ground Beef, 80% lean meat/20% fat, raw; Pork,
fresh, ground, raw; Chicken, broilers or fryers, meat and skin, raw; Milk, dry, whole; Spinach,
raw; Tomatoes, red, ripe, raw, year-round average; Lima Beans, large, mature seeds, raw; Peas,
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14. I've never really liked putting such specific cutoff points on initiation, promotion and pro-
gression of chronic disease, because these cutoff points for each stage of chronic disease are
completely arbitrary. What's important to know is that a chronic disease can be with us for
most of our lives, and if it progresses, it will do so in a very fluid, continuous manner.

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336 (1990): 37-39.

PART IV

Chapter 13

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6. American Council of Science and Health. 01/08/04. Accessed at http://www.achs.org/about/
index.html

7. Mindfully.org. 01/08/2004. Accessed at http://www.mindfully.org/Pesticide/ACSH-koop.htm

8. American Society for Nutritional Sciences. 01/08/04. Accessed at http://www.asns.org

Chapter 14

1. National Research Council. Diet, Nutrition and Cancer. Washington, DC: National Academy
Press, 1982.

2. United States Federal Trade Commission. "Complaint counsel's proposed findings of fact,
conclusions of law and proposed order (Docket No. 9175)." Washington, DC: United States
Federal Trade Commission, December 27, 1985.

3. Associated Press. "Company news; General Nutrition settles complaint." The New York Times
June 14, 1988: D5.

4. Willett W. "Diet and cancer: one view at the start of the millennium." Cancer Epi. Biom. Prev.
10 (2001): 3-8.

5. Belanger CF, Hennekens CH, Rosner B, et al. "The Nurses' Health Study." Am. J. Nursing
(1978): 1039-1040.

6. Marchione M. "Taking the long view; for 25 years, Harvard's Nurses' Health Study has sought
answers to women's health questions." Milwaukee Journal-Sentinel July 16, 2001: 01G.

7. Carroll KK. "Experimental evidence of dietary factors and hormone-dependent cancers."
Cancer Res. 35 (1975): 3374-3383.

8. ChenJ, Campbell TC, Li J, et al. Diet, life-style and mortality in China. A study of the character-
istics of 65 Chinese counties. Oxford, UK; Ithaca, NY; Beijing, PRC: Oxford University Press;
Cornell University Press; People's Medical Publishing House, 1990.

9. Hu FB, Stampfer MJ, Manson JE, et al. "Dietary protein and risk of ischemic heart disease in
women." Am.Joum. Clin. Nulr. 70 (1999): 221-227.

10. Holmes MD, Hunter DJ, Colditz GA, et al. "Association of dietary intake of fat and fatty acids
with risk of breast cancer." JAMA 281 (1999): 914-920.

11. U.S. Department of Agriculture. "Agriculture Fact Book." Washington, DC: U.S. Department
of Agriculture, 1998. cited in: Information Plus Nutrition: a key to good health. Wylie, TX:
Information Plus, 1999.

12. While the average percentage of calories derived from fat has gone down slightly, average
daily fat intake, in grams, has stayed the same or has gone up.

13. Information Plus. Nutrition: a key to good health. Wylie, TX: Information Plus, 1999.

396

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14. Wegmans.com. 01/19/04. Accessed ai http://www.wegmans. com/recipes

15. Mardiweb.com. "Cheesecake." 01/19/04. Accessed at http://mardiweb.com/lowfal/dessert.ht
m#Recipe000857

16. Anonymous. "Center to Coordinate Women's Health Study." Chicago Sun-Times October 12,
1992: 14N.

17. Prentice RL, Kakar F, Hursting S, et al. "Aspects of the rationale for the Women's Health
Trial. "J. Natl Cancer Inst. 80 (1988): 802-814.

18. Henderson MM, Kushi LH, Thompson DJ, et al. "Feasibility of a randomized trial of a low-
fat diet for the prevention of breast cancer: dietary compliance in the Women's Health Trail
Vanguard Study." Prev. Med. 19 (1990): 115-133.

19. Self S, Prentice R, Iverson D, et al. "Statistical design of the Women's Health Trial." Controlled
Clin. Trials 9 (1988): 119-136.

20. Armstrong D, and Doll R. "Environmental factors and cancer incidence and mortality in
different countries, with special reference to dietary practices." Int. J. Cancer 15 (1975):
617-631.

21. Campbell TC. "The dietary causes of degenerative diseases: nutrients vs foods." In: N. J.
Temple and D. R Burkitt (eds.), Western diseases: their dietary prevention and reversibility, pp.
119-152. Totowa, NJ: Humana Press, 1994.

22. White E, Shattuck AL, Kristal AR, et al. "Maintenance of a low-fat diet: follow-up of the
Women's Health Trial." Cancer Epi. Biom. Prev. 1 (1992): 315-323.

23. Willett WC, Hunter DJ, Stampfer MJ, et al. "Dietary fat and fiber in relation to risk of breast
cancer. An 8-year follow-up." J. Am. Med. Assoc. 268 (1992): 2037-2044.

24. Willett W. "Dietary fat and breast cancer." Toxicol. Sci. 52[Suppl] (1999): 127-146.

25. Hunter DJ, Spiegelman D, Adami H-O, et al. "Cohort studies of fat intake and the risk of
breast cancer — a pooled analysis." New Engl. J. Med. 334 (1996): 356-361.

26. Missmer SA, Smith-Warner SA, Spiegelman D, et al. "Meat and dairy consumption and breast
cancer: a pooled analysis of cohort studies." Int. J. Epidemiol. 31 (2002): 78-85.

27. Rockhill B, Willett WC, Hunter DJ, et al. "Physical activity and breast cancer risk in a cohort
of young women." J. Nat. Cancerlnst. 90 (1998): 1155-1160.

28. Smith-Warner SA, Spiegelman D, Adami H-O, et al. "Types of dietary fat and breast cancer: a
pooled analysis of cohort studies." Int.]. Cancer 92 (2001): 767-774.

29. Hunter DJ, Morris JS, Stampfer MJ, et al. "A prospective study of selenium status and breast
cancer risk. " JAMA 264(1 990) .1128-1131.

30. Smith-Warner SA, Spiegelman D, Yaun S-S, et al. "Intake of fruits and vegetables and risk of
breast cancer: a pooled analysis of cohort studies." JAMA 285 (2001): 769-776,

31. Mukamal KJ, Conigrave KM, Mittleman MA, et al. "Roles of drinking pattern and type of al-
cohol consumed in coronary heart disease in men." New Engl. J. Med. 348 (2003): 109-118.

32. Tanasescu M, Hu FB, Willett WC, et al. "Alcohol consumption and risk of coronary heart dis-
ease among men with Type 2 diabetes mellitus." J. Am. Coll Cardiol. 38 (2001): 1836-1842.

33. Smith-Warner SA, Spiegelman D, Yaun S-S, et al. "Alcohol and breast cancer in women. A
pooled analysis of cohort studies." JAMA 279 (1998): 535-540.

34. He K, Rimm EB, Merchant A, et al. "Fish consumption and risk of stroke in men." JAMA 288
(2002): 3130-3136.

35. Albert CM, Hennekens CH, O'Donnell CJ, et al. "Fish consumption and risk of sudden car-
diac death." JAMA 279 (1998): 23-28.

36. U.S. Department of Agriculture. "USDA Nutrient Database for Standard Reference." Wash-
ington, DC: U.S. Department of Agriculture, Agriculture Research Service, 2002. Accessed at
http://www.nal.usda.gov/fnic/foodcomp

37. Hu FB, Stampfer MJ, Rimm EB, et al. "A prospective study of egg consumption and risk of
cardiovascular disease in men and women." JAMA 281 (1999): 1387-1394.

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38. Hu FB, Manson JE, and Willett WC. "Types of dietary fat and risk of coronary heart disease:
a critical review."/. Am. Coll. Nutr. 20 (2001): 5-19.

39. Mitchell S. "Eggs might reduce breast cancer risk." United Press International Feb. 21, 2003

40. Steinmet2, K. A. and Potter, J. D. "Egg consumption and cancer of the colon and rectum." Eur.
J. Cancer Prev., 3: 237-245, 1994.

41. Giovannucci E, Rimm EB, Stampfer MJ, et al. "Intake of fat, meat, and fiber in relation to risk
of colon cancer in men." Cancer Res. 54 (1994): 2390-2397.

42. Fuchs CS, Giovannucci E, Coldit2 GA, et al. "Dietary fiber and the risk of colorectal cancer
and adenoma in women." New Engl. J. Med. 340 (1999): 169-176.

43. Higgirtson J. "Present trends in cancer epidemiology." Proc. Can. Cancer Conj. 8 (1969): 40-75.

44. Burkitt DP. "Epidemiology of cancer of the colon and the rectum." Cancer 28 (1971): 3-13.

45. Trowell HC, and Burkitt DP. Western diseases: their emergence and prevention. London: Butler
& Tanner, Ltd., 1981.

46. Boyd NF, Martin LJ, Noffel M, et al. "A meta-analysis of studies of dietary-fat and breast can-
cer risk." Brit./. Cancer 68 (1993): 627-636.

47. Campbell TC. "Animal protein and ischemic heart disease." Am. J. Clin. Nutr. 71 (2000):
849-850.

48. Hu FB, and Willett W. "Reply to TC Campbell." Am. J. Clin. Nutr. 71 (2000): 850.

49. Morris CD, and Carson S. "Routine vitamin supplementation to prevent cardiovascular dis-
ease: a summary of the evidence for the U.S. Preventive Services Task Force." Ann. Internal
Med. 139 (2003): 56-70.

50. U.S. Preventive Services Task Force. "Routine vitamin supplementation to prevent cancer and
cardiovascular disease: recommendations and rationale." Ann. Internal Med. 139 (2003): 51-55.

Chapter 15

1. Putman JJ, and Allshouse JE. "Food Consumption, Prices, and Expenditures, 1970-95."
Washington, DC: United States Department of Agriculture, 1997. Cited in: Information Plus.
Nutrition: a key to good health. Wylie, TX: Information Plus, 1999.

2. National Dairy Council. July 15, 2003. Accessed at http://www.nationaldairycouncil.org/
aboutus.asp

3. Dairy Management Inc. "What is Dairy Management Inc.?" February 12, 2004. Accessed at
http://www.dairycheckofT.corn/whatisdmi.htrn

4. Dairy Management Inc. Press release. "Dairy checkoff 2003 unified marketing plan budget
geared to help increase demand in domestic and international markets." Rosemont, 1L: Janu-
ary 24, 2003. Accessed at http://www.dairycheckoff.com/news/release-012403.asp

5. National Watermelon Promotion Board. January 12, 2004. Accessed at http://www.watermelon.org

6. Dairy Management Inc. "2001 Annual Report." Dairy Management, Inc., 2001. Accessed at
http://www.dairycheckoff.com/annualreport.htm/

7. United States Department of Agriculture. "Report to Congress on the National Dairy Pro-
motion and Research Program and the National Fluid Milk Processor Promotion Program."
2000. Accessed at http://www.ams.usda.gov/dairy/prb_intro.htm.IN

8. United States Department of Agriculture. "Report to Congress on the National Dairy Pro-
motion and Research Program and the National Fluid Milk Processor Promotion Program."
2003. Accessed at http://www.ams.usda.gov/dairy/prb/prb_rept_2003.htm

9. Nutrition Explorations. July, 2003. Accessed at http://www.nutritionexplorations.com

10. Powell A. "School of Public Health hosts food fight: McDonald's, dairy industry, dietary
reformers face off at symposium." Harvard Gazette: 24 October 2002. Accessed at http:
//www.news.harvard.edu/gazette/2002/10.24/09-food.html

11. Ha YL, Grimm NK, and Pariza MW. "Anticarcinogens from fried ground beef: heat-altered
derivatives of linoleic acid." Carcinogensis 8 (1987): 1881-1887.

398

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12. Ha YL, Storkson J, and Pariza MW. "Inhibition of benzo(a)pyrene-induced mouse forestomach
neoplasia by conjugated denoic derivatives of linoleic acid." Cancer Res. 50 (1990): 1097-1101.

13. Aydin R, Pariza MW, and Cook ME. "Olive oil prevents the adverse effects of dietary conju-
gated linoleic acid on chick hatchability and egg quality." J. Nutr 131 (2001): 800-806.

14. Peters JM, Park Y, Gonzalez FJ, et al. "Influence of conjugated linoleic acid on body com-
position and target gene expression in peroxisome proliferator-activated receptor alpha-null
mice." Biochim. Biophys. Acta 1533 (2001): 233-242.

15. Ntambi JM, Choi Y, Park Y, et al. "Effect of conjugated linoleic acid (CLA) on immune re-
sponses, body composition and stearoyl-CoA desaturase." Can. J. App\. Physiol. 27 (2002):
617-627.

16. Ip C, Chin SF, Scimeca JA, et al. "Mammary cancer prevention by conjugated dienoic deriva-
tive of linoleic acid." Cancer Res. 51 (1991): 6118-6124.

17. lp C, Cheng J, Thompson HJ, et al. "Retention of conjugated linoleic acid in the mammary
gland is associated with tumor inhibition during the post-initiation phase of carcinogenesis."
Carcinogensis 18 (1997): 755-759.

18. YaukeyJ. "Changing cows' diets elevates milks' cancer-fighting." Ithaca Journal November 12,
1996: 1.

19. Belury MA. "Inhibition of carcinogenesis by conjugated linoleic acid: potential mechanisms
of action.";. Nutr. 132 (2002): 2995-2998.

20. Ip C, Banni S, Angioni E, et al. "Conjugated linoleic acid-enriched butter fat alters mammary
gland morphogenesis and reduces cancer risk in rats." J. Nutr 129 (1999): 2135-2142.

21. Griinari JM, Corl BA, Lacy SH, et al. "Conjugated linoleic acid is synthesized endogenously
in lactating dairy cows by D 9 -desaturase." J. Nutr. 130 (2000): 2285-2291.

22. Ip C, Dong Y, Thompson HJ, et al. "Control of rat mammary epithelium proliferation by
conjugated linoleic acid." Nutr Cancer 39 (2001): 233-238.

23. Ip C, Dong Y, Ip MM, et al. "Conjugated linoleic acid isomers and mammary cancer preven-
tion." Nutr. Cancer 43 (2002): 52-58.

24. Giovannucci E. "Insulin and colon cancer." Cancer Causes and Control 6 (1995): 164-179.

25. Mills PK, Beeson WL, Phillips RL, et al. "Cohort study of diet, lifestyle, and prostate cancer."
Cancer 64 (1989): 598-604.

26. Search for keyword "lycopene" at http://www.ncbi.nlm.nih.gov

27. Christian MS, Schulte S, and HellwigJ. "Developmental (embryo-fetal toxicity/teratogenecity)
toxicity studies of synthetic crystalline lycopene in rats and rabbits." Food Chem. Toxicol. 41
(2003): 773-783.

28. Giovannucci E, Rimm E, Liu Y, et al. "A prospective study of tomato products, lycopene, and
prostate cancer risk." J. Nat. Cancer Inst. 94 (2002): 391-398.

29. Gann PH, and Khachik F. "Tomatoes or lycopene versus prostate cancer: is evolution anti-
reductionist?" J. Nat. Cancer Inst. 95 (2003): 1563-1565.

30. Tucker G. "Nutritional enhancement of plants." Curr. Opin. 14 (2003): 221-225.

31. He Y. Effects of carotenoids and dietary carotenoid extracts on aflatoxin B^induced mutagenesis
and hepatocarcinogenesis. Ithaca, NY: Cornell University, PhD Thesis, 1990.

32. He Y, and Campbell TC. "Effects of carotenoids on aflatoxin Bj-induced mutagenesis in S.
typhimurium TA 100 and TA 98." Nutr. Cancer 13 (1990): 243-253.

33. Giovannucci E, Ascherio A, Rimm EB, et al. "Intake of carotenoids and retinol in relation to
risk of prostate cancer." J. Nat. Cancer Inst. 87 (1995): 1767-1776.

34. U.S. Department of Agriculture. "USDA Nutrient Database for Standard Reference." Wash-
ington, DC: U.S. Department of Agriculture, Agriculture Research Service, 2002. Accessed at
http://www.nal.usda.gov/fnic/foodcomp

35. Eberhardt MV, Lee CY, and Liu RH. "Antioxidant activity of fresh apples." Nature 405 (2000):
903-904.

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Chapter 16

1. Food and Nutrition Board, and Institute of Medicine. "Dietary reference intakes for energy,
carbohydrates, fiber, fat, fatty acids, cholesterol, protein, and amino acids (macronutrients)."
Washington, DC: The National Academy Press, 2002. Accessed at http://www.nap.edu/
catalog/10490. html?onpi_newsdoc090502

2. National Academy of Sciences. Press Release. "Report offers new eating and physical activity
targets to reduce chronic disease risk." Sept. 5, 2002. Washington, DC: National Research
Council, Institute of Medicine. Accessed at http://www4.nationalacademies.org/news.nsf/
isbn/0309085373?OpenDocument

3. Wegmans Company. Recipe and nutrient facts. Accessed 2003. Available from http://
www.wegmans.com.

4. U.S. Department of Agriculture. "USDA Nutrient Database for Standard Reference." Wash-
ington, DC: U.S. Department of Agriculture, Agriculture Research Service, 2002. Accessed at
http://www.nal.usda.gov/fnic/foodcomp

5. The RDA has been expressed as a singular quantity of protein, as 0.8 grams of protein per
kilogram of body weight. Assuming a daily intake of 2,200 calories for a 70 kg person, this
0.8 grams is equivalent to about 10-11% of total calories: 70 kg X 0.8 gm/kg X 4 cal/gm X
1/2200 cal X 100 = 10.2%

6. Wright JD, Kennedy-Stephenson J , Wang CY, et al. "Trends in Intake of Energy and Macro-
nutrients - United States, 1971-2000." Morbidity and mortality weekly report 53 (February 6,
2004): 80-82.

7. Boseley S. "Sugar industry threatens to scupper WHO." The Guardian April 21, 2003

8. Brundtland GH. "Sweet and sour; The WHO is accused by the sugar industry of giving un-
scientific nutrition advice. But its recommendations are based on solid evidence, says Gro
Harlem Brundtland." New Scientist, May 03, 2003: 23.

9. International Life Sciences Institute. /LSI North America. Accessed February 13, 2004. Avail-
able from http://www.ilsina.org.

10. Kursban M. Commentary: conflicted panel makes Jor unfit guidelines. Physicians Committee
for Responsible Medicine. Accessed June, 2003. Available from http://www.pcrm.org/health/
commentary/commen tary0004.html.

11. Chaitowitz S. Court rules against VSDAs secrecy and failure to disclose conflict of interest in set-
ting nutrition policies. Physicians Committee for Responsible Medicine. Accessed January 27,
2004. Available from http://www.pcrm.org/news/health001002.html.

12. I have been for several years on the science advisory board of PCRM.

13. National Academy of Sciences, and Institute of Medicine. "Dietary Reference Intakes for
Energy, Carbohydrates, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids |sum-
mary statement]." Washington, DC: National Academy Press, September, 2002.

14. National Institutes of Health. February 2004. Accessed at http://www.nih.gov

15. National Institutes of Health. "National Institutes of Health. Summary of the FY 2005 Presi-
dent's Budget." February 2, 2004. Accessed at http://www.nih.gov/news

16. National Institutes of Health. NJH Disease Funding Table: Special Areas of Interest. Accessed
August 18, 2003. Available from http://www.nih.gov/news/findingresearchareas.htm.

17. Calculated from NIH Disease Funding Table: Special Areas of Interest. See previous reference.

18. National Cancer Institute. "FY 1999 Questions and Answers provided for the record
for the FY 1999 House Appropriations Subcommitee." July 15, 2003. Accessed at http:
//www3. cancer.gov/admin/fmb/1999QAs.htm

19. National Cancer Institute. FY 2001 Congressional Justification. Accessed March 2, 2004. Avail-
able from http^/www3.cancer.gov/admin/fmb/index.html.

20. Angell M. "The pharmaceutical industry — to whom is it accountable?" New Engl. J. Med. 342
(2000): 1902-1904.

400

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21. National Cancer Institute. FY 2004 Congressional Justification. Accessed 2003. Available from
http://www3.cancer.gov/admin/fmb/index/html.

22. Demas A. Food Education in the Elementary Classroom as a Means of Gaining Acceptance oj
Diverse Low Fat Foods in the School Lunch Program [PhD Dissertation]. Ithaca, NY: Cornell
University, 1995:325pp.

Chapter 17

1. AustokerJ. "The 'treatment of choice': breast cancer surgery 1860-1985." Soc. Soc. Hist. Med.
Bull.(London) 37 (1985): 100-107.

2. Naifeh SW. The Best Doctors in America, 1994-1995. Aiken, S C.: Woodward & White, 1994.

3. McDougall JA, and McDougall MA. The McDougall Plan. Clinton, NJ: New Win Publishing,
Inc., 1983.

4. Committee on Nutrition in Medical Education. "Nutrition Education in U.S. Medical
Schools." Washington, DC: National Academy of Sciences, 1985.

5. White PL, Johnson OC, and Kibler MJ. "Council on Foods and Nutrition, American Medical
Association — its relation to physicians." Postgraduate Med. 30 (1961): 502-507.

6. Lo C. "Integrating nutrition as a theme throughout the medical school curriculum." Am. ].
Clin. Nutr. 72(Suppl) (2000): 882S-889S.

7. Pearson TA, Stone EJ, Grundy SM, et al. "Translation of nutrition science into medical educa-
tion: the Nutrition Academic Award Program." Am. J. Clin. Nutr. 74 (2001): 164-170.

8. Kassler WJ. "Appendix F: Testimony of the American Medical Student Association." Wash-
ington, DC: National Academy of Sciences, 1985.

9. Zeisel SH, and Plaisted CS. "CD-ROMs for Nutrition Education." J. Am. Coll Nutr. 18 (1999): 287.

10. Two or three reputable agencies have also sponsored this program, but I suspect that the ad-
ministrators of these agencies felt it necessary to associate with a project in medical education
for their own purposes, regardless of the dubious list of other organizations.

11. http://viTvw.med.unc. edu/nutr/nim/FAQ.htm#anchorl97343

12. Weinsier RL, Boker JR, Brooks CM, et al. "Nutrition training in graduate medical (residency)
education: a survey of selected training programs." Am.]. Clin. Nutr. 54 (1991): 957-962.

13. Young EA. "National Dairy Council Award for Excellence in Medical/Dental Nutrition Edu-
cation Lecture, 1992: perspectives on nutrition in medical education." Am. ]. Clin. Nutr. 56
(1992): 745-751.

14. Kushner RF "Will there be a tipping point in medical nutrition education?" Am.]. Clin. Nutr.
77 (2003): 288-291.

15. Angell M. "Is academic medicine for sale?" New Engl]. Med. 342 (2000): 1516-1518.

16. Moynihan R. "Who pays for the pizza? Redefining the relationships between doctors and
drug companies 1: Entanglement." Brit. Med.Journ. 326 (2003): 1189-1192.

17. Moynihan R. "Who pays for the pizza? Redefining the relationships between doctors and
drug companies. 2. Disentanglement." Brit. Med.Journ. 326 (2003): 1193-1196.

18. Avom J, Chen M, and Hartley R. "Scientific versus commercial sources of influence on the
prescribing behavior of physicians." Am. J. Med. 73 (1982): 4-8.

19. Lurie N, Rich EC, Simpson DE, et al. "Pharmaceutical representatives in academic medical
centers: interaction with faculty and housestaff." J. Gen. Intern. Med. 5 (1990): 240-243.

20. Steinman MA, Shlipak MG, and McPhee SJ. "Of principles and pens: attitudes and practices
of medicine housestaff toward pharmaceutical industry promotions." Am.}. Med. 110 (2001):
551-557.

21. Lexchin J. "Interactions between physicians and the pharmaceutical industry: what does the
literature say?" Can.. Med. Assoc.]. 149 (1993): 1401-1407.

22. Lexchin J. "What information do physicians receive from pharmaceutical representatives?"
Can. Fam. Physician 43 (1997): 941-945.

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23. Baird P "Getting it right: industry sponsorship and medical research." Can. Med. Assoc. Joum.
168 (2003): 1267-1269.

24. Smith R. "Medical journals and pharmaceutical companies: uneasy bedfellows." Brit. Med.
Joum. 326 (2003): 1202-1205.

25. Chopra SS. "Industry funding of clinical trials: benefit or bias?"JAMA 290 (2003): 113-114.

26. Healy D. "In the grip of the python: conficts at the university-industry interface." Sci. Engi-
neering Ethics 9 (2003): 59-71.

27. Olivieri NE "Patients' health or company profits? The commericalization of academic re-
search." Sci. Engineering Ethics 9 (2003): 29-41.

28. Johnson L. "Schools report research interest conflicts." The Ithaca Journal October 24, 2002: 3A.

29. Agovino T. "Prescription use by children multiplying, study says." The Ithaca Journal Sept.
19, 2002: 1A.

30. Associated Press. "Survey: many guidelines written by doctors with ties to companies." The
Ithaca Journal Feb. 12, 2002

31. Weiss R. "Correctly prescribed drugs take heavy toll; millions affected by toxic reactions."
The Washington Post Apr. 15, 1998: A01.

32. Lasser KE, Allen PD, Woolhandler SJ, et al. "Timing of new black box warnings and with-
drawals for prescription medications." JAMA 287 (2002): 2215-2220.

33. LazarouJ, Pomeranz B, and Corey PN. "Incidence of adverse drug reactions in hospitalized
patients. "JAMA 279 (1998): 1200-1205.

Chapter 1 8

1. Macilwain G. The General Nature and Treatment oj Tumors. London, UK: John Churchill,
1845.

2. Williams H. The Ethics oj Diet. A Catena oj Authorities Deprecatory oj the Practice oj Flesh-Eat-
ing. London: F Pitman, 1883.

3. U.S. Census Bureau. "U.S. Popclock Projection." March, 2004. Accessed at hup://
www.census.gov/cgi-bin/popclock

4. Centers for Disease Control. "Prevalence of adults with no known risk factors for coronary
heart disease-behavioral risk factor surveillance system, 1992." Morbidity and mortality
weekly report 43 (February 4, 1994): 61-63,69.

5. Kaufman DW, Kelly JP, Rosenberg L, et al. "Recent patterns of medication use in the ambula-
tory adult population of the United States: the Slone survey." J. Am. Med. Assoc. 287 (2002):
337-344.

6. Flegal KM, Carroll MD, Ogden CL, et al. "Prevalence and trends in obesity among U.S.
adults, 1999-2000." JAMA 288 (2002): 1723-1727.

7. American Heart Association. "High blood cholesterol and other lipids — statistics." March,
2004. Accessed at http://www.americanheart.org/presenter.jhtml?identifier=2016

8. Wolz M, Cutler J, Roccella EJ, et al. "Statement from the National High Blood Pressure Edu-
cation Program: prevalence of hypertension." Am. J. Hypertens. 13 (2000): 103-104.

9. Lucas JW, Schiller JS, and Benson V. "Summary health statistics for U.S. Adults: National
Health Interview Survey, 2001." National Center for Health Statistics. Vital Health Stat.
10(218). 2004

10. Robbins J. The Food Revolution. Berkeley, California: Conari Press, 2001.

11. I strongly recommend reading John Robbins' "The Food Revolution," which convincingly
details the connection between your diet and the environment.

12. World Health Organization. "The World Health Report 1997: Press Release. Human and so-
cial costs of chronic diseases will rise unless confronted now, WHO Director-General says."
Geneva, Switzerland: World Health Organization, 1997. Accessed at http://www.who.int/
whr200 1/200 l/archives/1997/presse.htm

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13. Ornish, D., Brown, S. E., Scherwitz, L. W, BillingsJ. H., Armstrong, W T., Ports, T. A., McLa-
nahan, S. M., Kirkeeide, R. L., Brand, R. J., and Gould, K. L. "Can lifestyle changes reverse
coronary heart disease?" Lancet, 336: 129-133, 1990.

Esselstyn, C. B., Ellis, S. G., Medendorp, S. V, and Crowe, T. D. "A strategy to arrest and
reverse coronary artery disease: a 5-year longitudinal study of a single physician's practice."
]. Family Practice, 41: 560-568, 1995.

14. Vegetarian Resource Group. "How Many Vegetarians Are There?" March, 2004. Accessed at
http://www.vrg.org/journal/vj2003issue3/vj2003issue3poll.htm

15. Herman-Cohen V. "Vegan revolution." Ithaca Journal (reprinted from LA Times) Aug 11, 2003:
12A.

16. SabateJ, Duk A, and Lee CL. "Publication trends of vegetarian nutrition articles in biomedi-
cal literature, 1966-1995." Am. J. Clin. Nutr. 70(Suppl) (1999): 601S-607S.

Appendix A

1. BoydJN, Misslbeck N, Parker RS, et al. "Sucrose enhanced emergence of anatoxin B t (AFB^-
induced GGt positive rat hepatic cell foci." Fed. Proc. 41 (1982): 356 Abst.

2. Tannenbaum A, and Silverstone H. "Nutrition in relation to cancer." Adv. Cancer Res. 1
(1953): 451-501.

3. Youngman LD. The growth and development oj aflatoxin Bl-induced preneoplastic lesions, tu-
mors, metastasis, and spontaneous tumors as they are influenced by dietary protein level, type, and
intervention. Ithaca, NY: Cornell University, Ph.D. Thesis, 1990.

4. Youngman LD, and Campbell TC. "Inhibition of aflatoxin Bl-induced gamma-glutamyl
transpeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets:
evidence that altered GGT+ foci indicate neoplastic potential." Carcinogenesis 13 (1992):
1607-1613.

5. Horio F, Youngman LD, Bell RC, et al. "Thermogenesis, low-protein diets, and decreased de-
velopment of AFBl-induced preneoplastic foci in rat liver." Nutr. Cancer 16 (1991): 31-41.

6. Bell RC, Levitsky DA, and Campbell TC. "Enhanced thermogenesis and reduced growth rates
do not inhibit GGT+ hepatic preneoplastic foci development." FASEB ]. 6 (1992): 1395 Abs.

7. Miller DS, and Payne PR. "Weight maintenance and food intake." J. Nutr. 78 (1962): 255-262.

8. Stirling JL, and Stock MJ. "Metabolic origins of thermogenesis by diet." Nature 220 (1968):
801-801.

9. Donald P, Pitts GC, and Pohl SL. "Body weight and composition in laboratory rats: effects of
diets with high or low protein concentrations." Science 211 (1981): 185-186.

10. Rothwell NJ, Stock MJ, and Tyzbir RS. "Mechanisms of thermogenesis induced by low pro-
tein diets." Metabolism 32 (1983): 257-261.

11. Rothwell NJ, and Stock MJ. "Influence of carbohydrate and fat intake on diet-induced
thermogenesis and brown fat activity in rats fed low protein diets." J Nutr 117 (1987):
1721-1726.

12. Krieger E, Youngman LD, and Campbell TC. "The modulation of aflatoxin(AFBl) induced
preneoplastic lesions by dietary protein and voluntary exercise in Fischer 344 rats." FASEB J.
2 (1988): 3304 Abs.

Appendix B

1. Chen J, Campbell TC, Li J, et al. Diet, life-style and mortality in China. A study oj the character-
istics oj 65 Chinese counties. Oxford, UK; Ithaca, NY; Beijing, PRC: Oxford University Press;
Cornell University Press; People's Medical Publishing House, 1990.

2. There were eight-two mortality rates, but about a third of these rates were duplicates of the
same disease for people of different ages.

REFERENCES

403

3. This also means that very little or no useful information is obtained by including the values of
all the individuals in the county. There is only one disease rate for each county; thus it is only
necessary to have one number for any of the variables being compared with the disease rate.

4. Piazza A. Food consumption and nutritional status in the Peoples Republic of China. London:
Westview Press, 1986.

5. Messina M, and Messina V. The Dietitian's Guide to Vegetarian Diets. Issues and Applications.
Gaithersburg, MD: Aspen Publishers, Inc., 1996.

Appendix C

1. Holick ME In: M. E. Shils, J. A. Olson, M. Shike and e. al (eds.), Modem nutrition in health and
disease, 9th ed., pp. 329-345. Baltimore, MD: Williams and Wilkins, 1999.

2. Barger-Lux MJ, Heaney R, Dowell S, et al. "Vitamin D and its major metabolites: serum levels
after graded oral dosing in healthy men." Osteoporosis Int. 8 (1998): 222-230.

3. The biological half-life of storage vitamin D is 10-19 days, the time it takes for half of it to
disappear.

4. Colston KW, Berger U, and Coombes RC. "Possible role for vitamin D in controlling breast
cancer cell proliferation." Lancet 1 (1989): 188-191.

5. Nieves J, Cosman F, Herbert J, et al. "High prevalence of vitamin D deficiency and reduced
bone mass in multiple sclerosis." Neurology 44 (1994): 1687-1692.

6. Al-Qadreh A, Voskaki I, Kassiou C, et al. "Treatment of osteopenia in children with insulin-
dependent diabetes mellitus: the effect of 1-alpha hydroxyvitamin D3." Eur. J. Pediatr. 155

(1996) : 15-17.

7. Cantorna MT, Hayes CE, and DeLuca HE "1,25-Dihydroxyvitamin D 3 reversibly blocks the
progression of relapsing encephalomyelitis, a model of multiple sclerosis." Proc. National
Acad. Sci 93 (1996): 7861-7864.

8. Rozen F, Yang X-F, Huynh H, et al. "Antiproliferative action of vitamin D-related compounds
and insulin-like growth factor-binding protein 5 accumulation." J. Nat. Cancer Inst. 89

(1997) : 652-656.

9. Cosman F, Nieves J, Komar L, et al. "Fracture history and bone loss in patients with MS."
Neurology 51 (1998): 1161-1165.

10. Giovannucci E, Rimm E, Wolk A, et al. "Calcium and fructose intake in relation to risk of
prostate cancer." Cancer Res. 58 (1998): 442-447.

11. Peehl DM, Krishnan AV, and Feldman D. "Pathways mediating the growth-inhibitory action
of vitamin D in prostate cancer." J. Nutr. 133(Suppl) (2003): 2461S-2469S.

12. Zella JB, McCary LC, and DeLuca HE "Oral administration of 1 ,25-dihydroxyvitamin D 3
completely protects NOD mice from insulin-dependent diabetes mellitus." Arcfi. Biochem
Biophys. 417 (2003): 77-80.

13. Davenport CB. "Multiple sclerosis from the standpoint of geographic distribution and race."
Arch. Neurol. Pschiatry 8 (1922): 51-58.

14. Alter M, Yamoor M, and Harshe M. "Multiple sclerosis and nutrition." Arch. Neurol. 31
(1974): 267-272.

15. Van der Mei 1A, Ponsonby AL, Blizzard L, et al. "Regional variation in multiple sclerosis
prevalence in Australia and its association with ambivalent ultraviolet radiaion." Neuroepide-
miology 20 (2001): 168-174.

16. McLeod JG, Hammond SR, and Hallpike JE "Epidemiology of multiple sclerosis in Australia.
With NSW and SA survey results." Med. J. Austr 160 (1994): 117-122.

17. Holick ME "Vitamin D: a millenium perspective." J. Cell. Biocfiem. 88 (2003): 296-307.

18. MacLaughlin JA, Gange W Taylor D, et al. "Cultured psoriatic fibroblasts from involved and
uninvolved sites have a partial, but not absolute resistance to the proliferation-inhibtion ac-
tivity of 1,25-dihydroxyvitamin D/ Proc. National Acad. Sci 52 (1985): 5409-5412.

404

THE CHINA STUDY

19. Goldberg P, Fleming MC, and Picard EH. "Multiple sclerosis: decreased relapse rate through
dietary supplementation with calcium, magnesium and vitamin D." Med. Hypoth. 21 (1986):
193-200.

20. Andjelkovic Z, Vojinovic J, Pejnovic N, et al. "Disease modifying and immunomodulatory
effects of high dose la(OH)D 3 in rheumatoid arthritis patients." Clin. Exp. Rheumatol. 17
(1999): 453-456.

21. Hypponen E, Laara E, Reunanen A, et al. "Intake of vitamin D and risk of Type 1 diabetes: a
birth-cohort study." Lancet 358 (2001): 1500-1503.

22. Breslau NA, Brinkley L, Hill KD, et al. "Relationship of animal protein-rich diet to kidney
stone formation and calcium metabolism." J. Clin. Endocrinol. Metab. 66 (1988): 140-146.

23. Langman CB. "Calcitriol metabolism during chronic metabolic acidosis." Semin. Nephrol. 9
(1989): 65-71.

24. Chan JM, Giovannucci EL, Andersson S-O, et al. "Dairy products, calcium, phosphorus,
vitamin D, and risk of prostate cancer (Sweden)." Cancer Causes and Control 9 (1998):
559-566.

25. Byrne PM, Freaney R, and McKenna MJ. "Vitamin D supplementation in the elderly: review
of safety and effectiveness of different regimes." Calcified Tissue Int. 56 (1995): 518-520.

26. Agranoff BW, and Goldberg D. "Diet and the geographical distribution of multiple sclerosis."
Lancet 2(7888) (November 2 1974): 1061-1066.

27. Akerblom HK, Vaarala O, Hyoty H, et al. "Environmental factors in the etiology of Type 1
diabetes." Am. J. Med. Genet. (Semin. Med. Genet.) 115 (2002): 18-29.

28. Chan JM, Stampfer MJ, Ma J, et al. "Insulin-like growth factor-I (IGF-I) and IGF binding
protein-3 as predictors of advanced-stage prostate cancer." J Natl Cancer Inst 94 (2002):
1099-1109.

29. Cohen P, Peehl DM, and Rosenfeld RG. "The IGF axis in the prostate." Horm. Metab. res. 26
(1994): 81-84.

30. Doi SQ, Rasaiah S, Tack I, et al. "Low-protein diet suppresses serum insulin-like growth fac-
tor-1 and decelerates the progresseion of growth hormone-induced glomerulosclerosis." Am.
]. Nephrol. 21 (2001): 331-339.

31. Heaney RP, McCarron DA, Dawson-Hughes B, et al. "Dietary changes favorably affect bond
remodeling in older adults." J. Am. Diet. Assoc. 99 (1999): 1228-1233.

32. Allen NE, Appleby PN, Davey GK, et al. "Hormones and diet: low insulin-like growth factor-1
but normal bioavailable androgens in vegan men." Brit. J. Cancer 83 (2000): 95-97.

Index

7, 1 2-dimethybenz(a)anthracene
(DBMA), 65

academia, 311-13

acrylamide, 235

additives, food, 253

adverse drug reactions, 16, 335

affluence, diseases of. See diseases of

affluence
aflatoxin, 5, 236

binding to DNA, 51-53

children, 36

in com, 35-36

foci development, 54, 59

liver cancer, 21, 35-36, 49

low-protein diet, 53

in peanuts and peanut butter, 35-36

protein, 51-59

tumor development, 60-61
Agriculture, United States Department

of, 28
Alar, 43
alcohol, 281

alternative medicine, 252, 334
Alzheimer's disease, 218-22

See also cognitive impairment
American Cancer Society, 263-64, 267
American Council on Science and Health

(ACSH), 259-60
American Diabetes Association, 152

American Heart Association, 131
American Institute for Cancer Research

(AICR), 261-67
American Meat Institute, 290
amino acids, 29-30
aminotriazole, 44
Anderson, James, 151, 154
Angell, Marcia, 316-17, 333-34
angina, 113
angioplasty, 122, 124
animal-based diet, 21, 28

antioxidants, 92

blood cholesterol, 77-78, 80-81

breast cancer, 85-89, 285

calorie consumption, 367

comparison with plant-based
diet, 358

diabetes, 149-50

dietary fat, 83, 86

government promotion of, 258

heart disease, 117-19

historical basis, 344-45

hormones (reproductive), 88, 160,
160-61

IGF-1 (Insulin-like Growth Factor
1), 179

large bowel cancer, 170, 170-71
nutrition, 230, 230-32
prostate cancer, 178
tumor development, 66-67
in the United States, 274, 276-78

405

406

THE CHINA STUDY

vitamin D, 179-81

See also dairy foods
animal-based protein

biomarkers, 88-89

blood cholesterol, 80, 1 73

calcium, 205

cancer, 367

in China, 274

dietary fat, 276-78, 278

heart disease, 119,120

IGF-l (Insulin-like Growth Factor
D.367

kidney stones, 212-14, 213

osteoporosis, 205-8

quality of protein, 30

in the United States, 274

urinary calcium, 206, 214

vitamin D, 200, 365-67, 366
animal experimentation, 45, 48, 62-64,

67, 351-52
animal foods industry, 252, 255-68

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